Neurobiology of reproductive behavior 1 (325-340, 459-462)

 Perhaps we enjoy sex because sexual activity = reproduction = passing on genes

 Why reproduce sexually with a partner, not individually? = help rearing the child tgt & increase variation and
enable quick evolutionary adaptations to change in the environment, esp new viruses and parasites = correct
errors in a disadvantageous mutation in one gene and your mate has a disadvantageous mutation in a
difference gene, your children could have a normal copy of both genes
 Sex and Hormones
o Females = two X chromosomes; males = one X and one Y chromosomes
 Chromosomes determine sexual differentiation entirely through chromosomes?
o Male and female mammals start with same anatomy during early stage of prenatal development
 Both have Mullerian ducts (precursor to female internal structures) & Wolffian ducts
(precursor to male internal structures) & undifferentiated gonads that are on their way to
becoming either testes or ovaries
 If looking at an embryo at early development, cannot determine whether it is male
or female
 Later, the male SRY (sex-determining region on Y chr) gene on Y chr, causes primitive gonads
to develop into testes (sperm-producing organs) which produce androgens (testosterone;
hormones that are more abundant in males) that increase growth of testes, causing them to
produce more androgens and so forth
 Positive feedback cannot go on forever, but lasts for a period of time during early
development
 Androgens cause primitive Wolffian ducts to develop into seminal vesicles (saclike
structures that store semen) and vas deferens (duct from the testies into penis)
 Testes produce Mullerian-inhibiting hormone (MIH), which causes Mullerian ducts
to degenerate
 Final result = penis and scrotum
 Females do not have SRY gene, so their gonads develop into ovaries and Wolffian ducts
degenerate
 Ovaries do not produce MIH, so females’ Mullerian ducts develop and mature into
oviducts, uterus, and upper vagina
 Males’ testes produce more androgens than estrogens (hormones that are more abundant
in females), whereas the females’ ovaries produce more estrogens than androgens
 Adrenal glands produce both sex hormones that have similar/opposite effects
 They are steroid hormones, containing four carbon rings
o Exert effects in three ways
 1) bind to membrane receptors, like NT, exerting rapid effects
 2) enter cells and activate certain kinds of proteins in the cytoplasm
 3) bind to receptors that bind to chromosomes in nucleus, where
they activate or inactivate certain genes
 androgens + estrogens = categories of chemicals, not a specific chemical itself
o androgen = testosterone; estrogen = estradiol
o Progesterone (another predominantly female hormone) prepares uterus for
implantation of a fertilized ovum and promotes maintenance of pregnancy
o At first, believed that hormones account for all biological differences in males and females, but some
depend on control by X and Y chromosomes independently of hormones
 At least three genes on Y chromosome of males are active in specific brain areas, and at least
one gene on the X chromosome is active in the female brain
 In both humans and nonhumans, Y chr has many sites that alter expression of genes
on the other chr
 SO: Genes on X and Y chr produce sex differences in addition to those that we can
trace to androgens and estrogens
 Organizing effects of sex hormones
o If injected estrogens into adult males and androgens into adult females, could we make males act
like females and vice versa? NO
 But if injected early in life, stronger effects
o Organizing effects of sex hormones produce long-lasting structural effects
 During a sensitive period in early development, during first trimester of pregnancy for
humans, sex hormones determine whether the body develops female or male genitals =
more receptors = greater sensitivity around female nipples than male nipples
 Sex hormones produce additional organizing effects at puberty
o Surge of hormones at puberty = breast development, facial hair and penis
growth, changes in voice, male-female differences in hypothalamus and in
brain anatomy
 The changes developing at puberty persist throughout life, even after [] of sex
hormones declines
o Activating effects are more temporary, continuing only while a hormone is present or shortly
beyond
 Current hormone levels influence the degree of sex drive
 Burst of hormones during pregnancy produce complex, temporary effects of emotional
arousal, aggressive behavior, learning, and cognition
o The organizing effects set the stage for activating effects
 Organizing effects set up female hypothalamus such that later hormones can activate
menstrual cycle
o However, distinction b/w organizing and activating effects is not absolute, as a hormone can produce
a combination of temporary and longer-lasting effects; but still helpful
o In mammals, differentiation of external genitals and several aspects of brain development depend
mainly on level of testosterone, not estradiol
 A high level of testosterone, converted within cells to dihydrotestosterone, causes external
genitals to develop the male pattern, and a low level leads to female pattern
 Estradiol produces important effects on internal organs, but little effect on external genitals
o Human sensitive period of genital formation = first trimester of pregnancy
 At first, external genitals of males and females look the same
 As a male’s developing testes secrete testosterone, certain enzymes convert it to
dihydrotestosterone, which is more effective at promoting growth of penis
 If dihydrotestosterone levels are high, tiny genital tubercle grows and develops into a penis
 If levels are low, tubercle develops into a clitoris
 Also, depending on levels of testosterone and dihydrotestosterone, the embryo develops
either a scrotum (male) or labia (female)
o In rats, testosterone begins masculinizing external genitals during the last several days of pregnancy
and first few days after birth and then continues masculinizing them at a declining rate for the next
month
 A female rat injected with testosterone during this period = partly masculinized, just as if her
own body had produced the testosterone; her clitoris grows larger, approaches sexually
receptive females, mounts them, and makes copulatory thrusting movements rather than
arching back and allowing males to mount her
 SO: early testosterone promotes male pattern and inhibits female pattern
o Injecting a genetic male with estrogens produces little effect on external anatomy
 However, if he lacks androgens or androgen receptors, he develops the female-typical
pattern of anatomy and behavior
 That outcome could result from castration, a genetic deficiency of androgen
receptors, or prenatal exposure to drugs that interfere with androgen response
(alcohol, marijuana, haloperidol (antipsychotic), phthalates (chemicals in
manufactured products), cocaine, and even aspirin)
o Results depend on quantities and timing of exposure
 Although estradiol does not significantly alter a male’s external anatomy, it can produce
abnormalities of prostate gland, the gland that produces a fluid that accompanies and
protect sperm cells when ejaculated
 Some estradiol-like compounds prevalent in plastic bottles and cans
 SO: male development is vulnerable to many sources of interference
o OVERSTATEMENT: Nature’s default setting is to make every mammal a female unless told to do
otherwise; add early testosterone and become male; without testosterone, become female
regardless of the amount of estradiol or other estrogens
 A genetic female that lacks estradiol during early life develops approx. normal female
external anatomy but does not develop normal sexual behavior
 Even if injected estradiol as adult, show little sexual response toward either male or
female partners
 SO: Estradiol contributes to female development, including certain aspects of brain
differentiation, even if it is not important for external anatomy
o Sex differences in hypothalamus
 Sex hormones early in life also influence development in parts of hypothalamus, amygdala,
and other brain areas
 Sexually dimorphic nucleus (in anterior hypothalamus) is larger in males and
contributes to control of male sexual behavior in ways that vary from one species to
another
 Parts of female hypothalamus generate a cyclic pattern of hormone release, as in
the human menstrual cycle
o Male hypothalamus cannot; female hypothalamus that was exposed to extra
testosterone early in development cannot
 In rodents, testosterone exerts much of its organizing effect through which it enters a
neuron in early development and is converted to estradiol
 Testosterone and estradiol chemically very similar
o Aromatic compound: a ring of 6 carbon atoms containing 3 double bonds
o An enzyme found in brain can aromatize testosterone into estradiol
o Drugs that prevent testosterone from being aromatized to estradiol block
organizing effects of testosterone on sexual development and impair male
sexual behavior and fertility
 On the other hand, a female rodent’s estradiol fails to masculinize her hypothalamus
o During early sensitive period, immature mammals have a protein called
alpha-fetoprotein which binds with estradiol and prevents it from entering
cells, where it could produce musicalizing effects
o Because testosterone does not bind to alpha-fetoprotein, it enters neurons
where enzymes convert it into estradiol
 Testosterone is a way of getting estradiol to its receptors when
estradiol circulating in the blood is inactivated
 SO: Injecting a large amount of estradiol actually masculinizes a
female rodent’s development / a female that lacked alpha-
fetoprotein would be masculinized by her own estradiol
 However, in primates such as humans, mechanism is different
 Testosterone enters neurons where it exerts its
masculinizing effects directly, and it does not have to be
aromatized to estradiol
 But similarity is that in both cases, testosterone masculinizes
the brain
o Sex differences in child behavior
 Some children have a stronger preference for boys’ or girls’ activities than others do, and
their preferences tend to be consistent over time (at the age of 3 => 13)
 This pattern results from socialization, as most parents give their sons and daughters
different sets of toys
 But not the whole story; predisposition for boys and girls to prefer different types of
toys but alternative explanation is that girls mature faster, so maybe it was harder
for boys to show preference (looked at two sets of toys equally)
 Gender differences in monkeys’ preferences towards toys as well, but not as strong as
humans
 Prenatal injections of testosterone to female monkey fetuses led to increased masculine-
type play after they were born
  Chemicals in mother’s blood during pregnancy (testosterone)
 Girls who had been exposed to higher testosterone levels in prenatal life showed
slightly elevated preferences for boys’ toys
o Anatomically normal
 Girls who have higher testosterone levels in early infancy spent more time than
average playing with toy trains
 Boys with higher testosterone levels spent less time than other boys playing with
dolls
 Phthalate levels in pregnant women
 Phthalates (from perfumes, hair spray, and food packaging) inhibit testosterone
production
 Sons with high phthalate levels showed less interest in typical boys’ toys and more
interest in typical girls’ toys
 SO: how much a child plays with boys’ toys is increased by prenatal exposure to testosterone
and decreased by prenatal exposure to phthalates
 SO: prenatal hormones, especially testosterone, alter the brain in ways that influence
differences b/w boys and girls in their activities and interests
 However, prenatal hormones combine forces with rearing experiences
 Multiplier effect: parents provide more of the kind of toy that the child showed a
preference for and more opportunities to strengthen the preference
 Activating effects of sex hormones
o At any time in life, current levels of testosterone or estradiol exert activating effects, temporarily
modifying behavior
 But behavior can also influence hormonal secretions (when doves court each other)
 In addition to sex hormones, pituitary hormone oxytocin is also important for reproductive
behavior
 Stimulates contractions of uterus during baby delivery
 Stimulates mammary gland to release milk
 Sexual pleasure at orgasm; a relaxation state shorty after orgasm
o oxytocin responsible for calmness and lack of anxiety after orgasm
o Males
 Testosterone essential for male sexual arousal acts by increasing touch sensitivity in penis
 Sex hormones also bind to receptors that increase responses in parts of
hypothalamus, including ventromedial nucleus, medial preoptic area (MPOA), and
anterior hypothalamus
 Testosterone primes MPOA to release dopamine, and MPOA neurons release
dopamine strongly during sex; more dopamine, more copulation
o Castrated male rats produce normal amounts of dopamine in MPOA but do
not release it in presence of receptive female = no copulation
 In moderate [], dopamine stimulates type D1 and D5 receptors, facilitating erection
of penis and sexually receptive postures in female
 In higher [], dopamine stimulates D2 receptors = orgasm
 SO: dopamine stimulates sexual activity
 Serotonin inhibits it by blocking dopamine release
o Antidepressant drugs increase serotonin activity, and side effects is
decreased sexual arousal
 Married men or men living with a woman = low testosterone levels than single men
 1) Marriage = decreased testosterone levels cus of decreased need to compete for a
sexual partner
o Increased testosterone levels at the time of divorce
 2) Men with lower testosterone levels are more likely to marry and remain married
o Single women have higher testosterone levels than married women
o Both men and women with higher testosterone levels are more likely to
seek additional sex partners even after marriage
 Castration = low testosterone = decreases male sexual interest and activity
 However, low testosterone NOT EQUAL TO impotence (inability to have an erection)
 o Common cause is impaired blood circulation in older men
 Viagra (sildenafil) increases male sexual ability by prolonging effects
of nitric oxide, which increase blood flow to penis (and to brain as
well)
 Testosterone reduction to control sex offenders
 But got to continue taking drugs
 Drawback: testosterone deprivation, weight gain, diabetes, and depression
o Females
 Menstrual cycle: a woman’s hypothalamus and pituitary interact with ovaries; periodic
variation in hormones and fertility over 28 days
 After the end of menstrual period, anterior pituitary releases follicle-stimulating
hormone (FSH) that promotes growth of a follicle in ovary
 Follicle nurtures the ovum (egg cell) and produces estrogen, including estradiol
 Toward the middle of menstrual cycle, follicle builds up more and more receptors to
FSH, so even though actual [] of FSH in blood is decreasing, its effects on follicle
increase
o As a result, follicle produces increasing amounts of estradiol
o The increased release of estradiol causes an increased release of FSH and
surge in release of luteinizing hormone (LH) from anterior pituitary
o FSH and LH cause follicle to release an ovum
 Remnant of follicle (corpus luteum) release hormone progesterone, which prepares
uterus for implantation of fertilized ovum and inhibits release of LH
 If the woman is pregnant, estradiol and progesterone levels continue to increase
o If not pregnant, both hormones decline, the lining of uterus is cast off
(menstruation), and cycle begins again
 Consequence of high estradiol and progesterone during pregnancy = fluctuating activity at
serotonin 3 (5HT3) receptor, responsible for nausea
 Increased sensitivity to nausea = minimize risk of eating sth harmful to fetus
 Birth-control pills interfere with usual feedback cycle b/w ovaries and pituitary
 Combination pill contains estrogen and progesterone, preventing surge of FSH and
LH that would otherwise release an ovum
 Estrogen-progesterone combo thickens mucus of cervix, making harder for a sperm
to reach the egg, and prevents an ovum, if released, from implanting in the uterus
 But does not protect against sexually transmitted diseases (AIDS or syphilis)
 In female rats, a combo of estradiol and progesterone = most effective for enhancing sexual
behavior
 Estradiol increases sensitivity of pudendal nerve, which transmits tactile stimulation
from vagina and cervix to brain
 For humans, frequency of sexual intercourse correlated with amount of testosterone that
women produced at periovulatory period (highest sexual desire that in turn influences
behavior), the days around the middle of menstrual cycle, when fertility is highest (highest
blood levels of pituitary hormones (FSH & LH) + steroids (Estradiol & Progesterone later in
midluteal phase)
 But day-to-day sexual desire correlated strongly with changes in levels of estradiol,
not testosterone
o Many women report a drop in a sexual desire after surgical removal of their
ovaries, resulting in lower estradiol levels
o Increasing estrogen levels 9-15 days after menstruation towards
periovulatory period = feeling “sexy”
 Women preferred more masculine faces at the time of ovulation
 SO: hormones associated with fertility move women’s mate preferences toward
men who look and act more masculine
 SO: estrogen levels increase during the days leading up to the middle of menstrual
cycle; lowest during and just after menstruation
 SO: in terms of neurotransmitter activity, erection depends on one set of dopamine
receptors, and orgasm depends on different dopamine receptors
 o Effects of sex hormones on nonsexual characteristics
 Prenatal androgens and estrogens influence brain development
 E.g., which neurons survive and which synapses form
 Both androgens and estrogens stimulate brain areas important for memory
 Some brain regions larger in men or women
 However, relationship b/w brain differences and behavioral differences is mere
speculation
 Women better at recognizing facial expressions of emotions?
 After women received testosterone, most became less accurate at recognizing facial
expressions of anger; the effect was temporary
 SO: testosterone interferes with attention to emotional expressions
 Parental behavior (rodents)
o Hormonal changes during pregnancy prepare a female mammal to provide milk and prepare her to
care for the young
 Eats and drinks more
 Become less fearful and more aggressive
 Mother rat increases secretion of estradiol and prolactin while decreasing production of
progesterone
 Prolactin necessary for milk production and maternal behavior such as retrieving the
young when they wander away from the nest & inhibits sensitivity to leptin, eating
more than usual
o Also changes pattern of hormone receptors
 Later in pregnancy, her brain increases sensitivity to estradiol in areas responsible for
maternal behavior and attention to the young, including medial preoptic area and anterior
hypothalamus
 POA/AH also important for temperature regulation, thirst, and sexual behavior
 Vasopressin hormone made in hypothalamus and secreted by posterior pituitary gland
important for social behavior, facilitating olfactory recognition of other individuals
 Male prairie voles which secrete much vasopressin establish long-term pair bonds
with females and help rear their young
o A male meadow vole with low vasopressin mates with a female and ignores
her
 Sitting in the middle of his recent mate and new female
 But can manipulate the activity of a single gene responsible for
vasopressin in hypothalamus and alter social behavior
 Although rodent maternal behavior depends on hormones for the first few days, become
less dependent later
 If a female that has never been pregnant is left with baby rats, ignores them first but
gradually becomes more attentive
o Does everything for them except to nurse them
o This experience-dependent behavior does not require hormonal changes
and occurs even in rats that had their ovaries removed
 Humans are not the only species in which a mother can adopt young
w/o first going thru pregnancy
 Mother becomes accustomed to the odors of babies
 Infant rats release chemicals that stimulate the mother’s vomeronasal organ, which
responds to pheromones
o But oddly, their pheromones stimulate aggressive behaviors that interfere
with maternal behavior
 However, for a mother that has just gone thru pregnancy, this
interference does not matter cus her hormones primed medial
preoptic area so strongly that it overrides competing impulses
 A female w/o hormonal priming rejects the young, however,
until she becomes familiar with their smell
 Why do mammals need two mechanisms (hormonal-dependent and one not)?
  In the early phase, hormones (prolactin and estradiol) compensate for mother’s lack
of familiarity with the young
 In the later phase, experience maintains the maternal behavior even though
hormones start to decline
 In humans, hormonal changes during pregnancy and delivery = produce milk;
otherwise, hormones might seem unimportant for parental behavior
 Both men and women who have never gone thru pregnancy can adopt children and
become parents
o However, possible that hormones influence the quality of parental care to
some extent
o In nonhuman mammals, mothers with a deficiency of alpha type of estradiol
receptor provide poor maternal care
o Humans show genetic variation in their alpha estrogen receptors
 Women with one of the genetic variants were more likely to treat
children harshly
 A correlation between fathers’ hormones and their behavior toward the young
o Low testosterone and high prolactin = increased care for children
o But these are correlational data; do not know to what extent the hormones
are the cause of men’s behavior and to what extent they are the result
 Social behavior: distinguishing characteristics of humans
o Infer what someone else knows or intends to do
o Teach one another
o Social neuroscience: the study of how genes, chemicals, and brain areas contribute to social
behavior
 The biology of love
o Pictures of the person you love will produce increased activation of certain brain areas associated
with reward, in ways similar to the high people report from addictive drugs
 Viewing a photo of your beloved activates hippocampus
 Thinking about someone you love evokes memories
 Love combines motivations, emotions, memories, and cognitions
o Oxytocin and the closely related hormone vasopressin
 Women release much oxytocin during and after childbirth
 Stimulates contractions of uterus and breast to produce milk
 Tends to promote maternal behavior and pair bonding in mammalian species
 Both men and women release it during sexual activity
 “love hormone”; love-enhancing, love-magnifying
 Oxytocin passes directly from nasal cavity to brain and exerts effects about half an hour later
after sprayed
 Didn’t increase attraction to everyone, but just to someone already loved
 Stood far away from a new female; enhanced a man’s fidelity to his partner,
decreasing his willingness to face the temptation of another attractive women
 Helps recognize facial expressions of emotion
 Oxytocin’s effect on social relations depends on who the other people are
 Increases conformity and trust to the opinions of your in-group but not to the
opinions of out-group
 Not always pro-social; when people perceive themselves as being threatened,
oxytocin increases attention to possible dangers, increasing anger, distress, and
negative reactions, especially to strangers
 SO: oxytocin increases attention to important social cues
o Greater attention to facial expressions and stronger positive responses to
your beloved, but increased wariness when you have reason to doubt
someone
 Empathy and altruism
o Helpfulness depends on empathy, the ability to identify with other people and feel their pain almost
as if it were your own
 Stronger in humans than in other species
  The ability to take someone else’s perspective depends on an area where the temporal
cortex meets the parietal cortex
 But no brain area concerns itself only with empathy and moral behavior, and many
areas of brain contribute
 Most people tend to be more generous toward those they see similar
 But the strength of in-group bias varies among individuals
o Even rats show in-group bias
o People vary in degree of empathy and altruism
 Variation correlates with brain activity
 Vary in the arousal of dorsomedial prefrontal cortex
 Psychopathic traits = do understand that others will suffer but emotional areas of the brain
show weak activation when trying to imagine someone else’s experience
 Lack empathic identification that would let them understand how others will feel

Neurobiology of reproductive behavior 2 (341-353)

 Evolutionary interpretations of mating behavior

o Charles Darwin’s theory of evolution by natural selection: individuals whose genes help them survive
will produce more offspring, and the next generation will resemble those with the favorable genes
 Second part: sexual selection = genes that make an individual more appealing to the other
sex will increase the probability of reproduction, and therefore the next generation will
resemble those who had these genes
 Can go only so far if it starts to interfere with survival
o Interest in multiple mates
 More men than women seek opportunities for casual sexual relationships
 1) be loyal to one woman and devote all of your energies
 2) or mate with many women that some of them can raise your babies w/o your
help
 But women go through pregnancy for 9 months for a single child
o Evolution may have predisposed men to be more interested in multiple
mates than women
o But a woman sometimes gains from having multiple sex partners as well
 Overall, no direct evidence that genes influence people’s
preferences for one mate or many
o What men and women seek in a mate
 Women prefer a mate who is likely to be a good provider of food and other requirements
 Most women tend to be cautious during courtship
 Men tend to have a stronger preference for a young partner
 Young women are likely to remain fertile longer than older women
 For women, older men have enough financial resources
 These preferences come from a strong learned environment from cultures, but maybe
genetics too
 If women financially independent, choose a mate who’s close to her own age, not
based on wealth
o Differences in jealousy
 Men have been more jealous of a wife
 If a man is to pass on his genes, he needs to be sure that the children he supports
are his own
o An unfaithful wife threatens that certainty
 Jealousy varies among cultures
o More upset by their partner’s becoming emotionally close to someone else
than by sexual affair
o Evolved or learned?
 In many species, a male defends his sexual access to one or more females, and females show
little response if her male sexually approaches male
 Evolutionary selection generally noncontroversial
  For us, it is less clear about men being interested in multiple mates and being more jealous
than women
 Due to ethical implications
 Scientific data not conclusive on how much our behavior is evolutionarily guided and
how much is learned
 Culture shows both similarities and differences in behavioral tendencies
 Our behavioral tendencies are a product of evolution, but not clear to what extent
evolution micromanages human behavior
 Gender identity and gender differentiated behaviors
o Coral gobies have gender switches
 People do not have this but have variations in sexual development
o Gender identity: what we consider ourselves to be; human characteristics
 Sex differences (biological differences between males and females) vs. gender differences
(differences that result from people’s thinking about themselves; human characteristic)
 Gender identity depends mainly on the way people rear their children
 But biological factors, especially prenatal hormones, are important also
o Intersexes
 Hermaphrodites: anatomies intermediate b/w male and female, or show a mixture of both
anatomies
 True hermaphrodite has some testicular and some ovarian tissue; rare
o Release two ova, each fertilized by a different sperm, which unite instead of
becoming twins = if one of the ova had an XX chr pattern and the other had
XY, the resulting child has some XX and XY cells
 Some are fertile as either male or female; not both
 So can’t impregnated himself/herself
 Some develop an intermediate appearance due to atypical hormone pattern
o Testosterone masculinizes genitals and hypothalamus in early development
o A genetic male with low testosterone or a deficiency of testosterone
receptor may develop a female or intermediate appearance
o A genetic female exposed to more testosterone can be partly masculinized
 The most common cause of this condition = congenital adrenal hyperplasia (CAH), meaning
overdevelopment of adrenal glands from birth
 Ordinarily, adrenal gland has a negative feedback relationship with pituitary gland
 Pituitary secretes ACTH, which stimulates adrenal gland
 Cortisol released from adrenal gland feeds back to decrease the release of ACTH
 Some have a genetic limitation in ability to produce cortisol = pituitary fails to
receive much cortisol as a feedback signal, continues to secrete more ACTH, causing
adrenal gland to secrete larger amounts of other hormones, including testosterone
o SO: female genetically deficient in the ability to produce cortisol = pituitary
gland doesn’t receive negative feedback signals and therefore continues
stimulating adrenal gland = produce large amounts of testosterone
o Male = no big deal; female = develop masculinization of their external
genitals (ovaries and other internal organs less affected)
 E.g., intermediate b/w clitoris and penis and swellings that appear
intermediate b/w labia and scrotum
 These children given medical treatments to bring adrenal
hormones within normal levels
o Or surgery
 Intersexes: people whose sexual development is intermediate
o Disorders of sexual development
o Interests and preferences of CAH girls
 Policy was to raise most intersexes as girls cus can undergo a surgery
 But their behavior masculinized as well
 Girls with CAH were intermediate b/w preferences of boys and girls w/o CAH
o More toys than normal girls but less toys than normal boys
o Parents let them play with whatever they wanted to play with
  Perform better on spatial mechanical skills, like boys do
 Interests are intermediate b/w male and female adolescents
o Read more sports magazines and fewer style magazines
o More physical aggression than women and less interest in infants
o More interested in rough sports and have male-dominated occupations
o SO: prenatal and early postnatal hormones influence people’s interests as
well as the physical development
o Testicular feminization
 Androgen insensitivity or testicular feminization= people with XY chr and produce normal
amounts of androgens (+ testosterone) but lack the receptor that enables androgens to
activate genes; cells do not respond to androgens
 Smaller penis or genitals like female’s
 Breasts develop and hips broaden but no menstrual cycle
o Has internal testes instead of ovaries and a uterus
o Pubic hair sparse or absent
o Psychologically female 
o Issues of gender assignment and rearing
 Girls with CAH look like normal females or intermediate b/w male and female
 Cloacal exstrophy = a defect of pelvis development = small penis
 But normal levels of testosterone in prenatal development
 Doctors began recommending that they should be reared as a girl
 Easier to reduce an enlarged clitoris to normal than expand it to penis size
 After the surgery, the child looks female
 But some with cloacal exstrophy reared as girls develop typical male interests
 Girls with CAH after surgery (reduced clitoris) experiences urinary incontinence and
lack of orgasm; no romantic attraction to men
 New recommendations:
 Be honest with intersexed person and do nth w/o their informed consent
 Identify the child as male or female based mainly on predominant external
appearance; don’t make everyone a female
 Rear the child as consistently as possible, but be prepared that the person might
later be sexually oriented toward males, females, both, or neither
 Do not perform surgery but if made an informed request, then it’s appropriate
o Discrepancies of sexual appearance
 Genetic males fail to produce 5-alpha-reductase 2, an enzyme that converts testosterone to
dihydrotestosterone which is more effective for masculinizing external genitals
 At birth look like a female and reared as a female
 But their brains had been exposed to male levels of testosterone during early
development
 At puberty, testosterone increases sharply and the result is growth of penis and
scrotum
 Okay, I guess I’m a boy now; the girl-turned-boy developed a male gender identity
and directed interest toward females
o Brains had been exposed to male levels of testosterone from prenatal life
onward
 Another boy had to be circumcised and then reared as a girl after
 After puberty, found something wrong with himself
 Biological predisposition had won out over the family’s attempts to rear the child as
a girl
 Neither hormones nor rearing patterns do not have complete control
 Sexual orientation
o Homosexual behavior in animal species as well, when they cannot find an opposite sex or when they
have hormonal abnormalities
o People discover sexual orientation, and not choose it
 Men discover early; women are slower
 Early masculine-type behaviors are poor predictors of sexual orientation in women
  Men rarely switch their sexual orientation as opposed to women
 Biological predisposition seems stronger for men
o Behavioral and anatomical differences
 Heterosexual men are slightly taller and heavier than homosexual men
 Prepulse inhibition ordinarily stronger in men; homosexual women slightly shifted in the
male direction compared to heterosexual women
o Genetics
 Sexual orientation is a genetic condition, but the size of that contribution is uncertain
 If one twin is homosexual, the probability for the other to be homosexual is higher for a
monozygotic twin than dizygotic twin
 Concordance for homosexual orientation higher for monozygotic but varies
depending on countries considerably
 Not that homosexuality is more common in monozygotic than dizygotic; it’s the
concordance – the probability that both twins have the same sexual orientation
 Could not find a particular gene that might be linked to sexual orientation
 Maybe a gene on the X chromosome, which man receives from his mother
o Higher incidence of homosexuality among the maternal than parental
relatives of homosexual men
o But conflicting findings; so unlikely that any gene on the X chromosome
plays a major role
o An evolutionary question
 Average homosexual man has 1/5 as many children as the average heterosexual man
 if a homosexual orientation depends on certain genes, why hasn’t evolution selected
strongly against those genes?
 1) Genes for homosexuality are maintained by kin selection
o Even if homosexual people do not have children themselves, they might do
a wonderful job of helping their brothers and sisters rear children
 2) Genes that produce male homosexuality might produce advantageous effects in
their relatives, increasing their probability of reproducing and spreading the genes
 3) Homosexuality relates to epigenetics produced by an environmental event rather
than changes in DNA sequence
o acetyl or methyl group activate or inactivate a gene
o some epigenetic changes persist in generations
o So no gene for sexuality but a hereditary effect
o Prenatal influences
 Adult hormone levels do not explain sexual orientation
 Homosexual and heterosexual men/women have nearly the same hormone levels
 But sexual orientation depends on testosterone during sensitive period of brain
development
o Animal studies shown that prenatal or early postnatal hormones can
produce organizing effects on both external anatomy and brain
development
 Probability of a homosexual orientation is slightly higher among men who have older
brothers
 What matters is the number of biological older brothers, not stepbrothers or
adopted brothers; the influence does not stem from social experiences
 The key is how many previous times the mother gave birth to a son
o Mother’s immune system sometimes reacts against a protein in a son and
then attacks subsequent sons enough to alter their development
 Later-born homosexual men tend to be shorter than average
 Stress on the mother during pregnancy
 Prenatal stress alters sexual development in laboratory animals
o Sons had normal male anatomy but in adulthood often responded to
presence of another male by arching their backs in the typical rat female
posture for sex
 o Most males that were subjected to either prenatal stress or alcohol
developed male sexual behavior + female sexual behaviors, but those who
were subjected to both decreased male sexual behaviors
 Prenatal stress and alcohol may alter brain development
o Stress releases endorphins, which can antagonize the effects of testosterone
on the hypothalamus
o Also elevates levels of certain adrenal hormones (corticosterone in rats,
cortisol in human) that decrease testosterone release
o Long-term effects of either prenatal stress or alcohol include several
changes in structure of CNS, making the affected males’ anatomy closer to
that of females
 So what influences account for differences in sexual orientation?
 Not the same in all instances
 Genetic or epigenetic factors contribute, as well as prenatal environment
 Later experiences probability contribute too, but know little about the types of
experience that would be most decisive
o Brain anatomy
 On average, left and right hemispheres of cerebral cortex are nearly equal size in
heterosexual females whereas the right hemisphere is a few percent larger in heterosexual
male
 Homosexual males resemble heterosexual females
 Homosexual females are intermediate b/w heterosexual females and males
 In heterosexual females, left amygdala more widespread connections than right amygdala
whereas heterosexual males have right amygdala that has more widespread connections
 Homosexual males resemble heterosexual females and homosexual females are
intermediate
 Anterior commissure is larger in heterosexual women than in heterosexual men
 In homosexual men, as large as women, or perhaps even larger
 SCN also larger in homosexual men than in heterosexual men
 BUT 1) don’t know whether these brain differences are causes or effects of sexual
orientation 2) easy to publish results even if the difference was unpredicted, small, and hard
to explain
 Third interstitial nucleus of anterior hypothalamus (INAH-3)
 More than twice as large in heterosexual men as in women
 This area has more cells with androgen receptors in men than in women
 Plays a role in sexual behavior
 Mean volume of INAH-3 larger in heterosexual men than in heterosexual women or
homosexual men
o Cause of death (AIDS) has no clear relationship to the results
o Substantial amount of difference among individual; cannot be confident
about this
o SO: INAH-3 volume does not depend on AIDS but on sexual orientation
 Later study found that INAH-3 nucleus slightly larger in heterosexual men than
homosexual men
o But homosexual men had a larger INAH-3 nucleus than heterosexual women
o Among heterosexual men or women, INAH-3 nucleus was larger in those
who were HIV negative than those who were HIV positive, but if we look at
only HIV-positive men, there’s a difference in the hypothalamus b/w
heterosexual and homosexual men
o Heterosexual men had larger neurons than homosexual men but about the
same number
 this study nor the previous study included homosexual females
o INAH-3 larger in heterosexual males than in male-to-female transsexuals
(people born as males who changed their identities to female)
 Do differences in hypothalamus influence sexual orientation, or vice versa?
 o In sheep, at least, anatomical differences appear before any sexual behavior;
so cause than a result
o Not sure about humans

Neurobiology of emotional behaviors 1 (355-370)

 Emotion is a difficult topic cus implies conscious feelings that we cannot observe
o Talk about emotional behaviors instead
 Distinguishing between motivation and emotion is difficult; maybe no real difference
o Emotion: cognitive evaluations, subjective changes, autonomic and neural arousal, and impulses to
action
 Has components including cognitions, actions, and feelings
o Motivation: an internal process that modifies the way an organism responds to a certain class of
external stimuli
 Emotions and autonomic arousal
o Emotional situations arouse autonomic system, both sympathetic and parasympathetic
 SNS stimulates heart and inhibits stomach and intestines
 Simulates fight-or-flight activities and inhibits vegetative activities
 PNS increases digestion and other processes that save energy and prepare for later events
 But most situations evoke a combo of both
 Nausea associated with sympathetic stimulation of stomach and parasympathetic
stimulation of intestines and salivary glands
 James-Lange theory: autonomic arousal and skeletal actions come first and feel emotion
later (frightening situation = running away, increased heart rate, etc. = fear)
 You feel afraid because you run away and you feel angry because you attack
 An emotion includes cognitions, actions, and feelings
o Cognitive (appraisal) comes first and that leads to action such as running
away and that in turn leads to feeling
 According to this theory, people with weak autonomic or skeletal responses should
feel less emotion and causing or increasing someone’s responses should enhance an
emotion
o Is physiological arousal necessary for emotional feelings?
 People with damage to spinal cord report experiencing emotions
 Pure autonomic failure: output from autonomic nervous system to body fails, either
completely or almost completely
 Heart beat continues but nervous system no longer regulates it
o Does not react to stressful experiences with changes in heart rate, blood
pressure, or sweating
o But still report having same emotions and little difficulty identifying what
emotion a character would probably experience
 But feel emotions less intensely than before
 Refer to cognitive aspect mainly; and decreased emotional
feeling = consistent with the theory
 Botulinum toxin (BOTOX) blocks transmission at synapses and nerve-muscle junctions
 Paralyzes muscles for frowning and remove frown lines on faces
 Weaker than usual emotional responses
o Feeling a body change is important for feeling an emotion
 People with damage to right somatosensory cortex have normal autonomic responses to
emotional music but report little subjective experience
 People with damage to part of prefrontal cortex have weak autonomic responses
but normal subjective responses
 Suggest a lack of connection b/w autonomic responses and subjective experience
 Subjective experience could be more cognition than feeling
o Is physiological arousal sufficient for emotions?
 Panic attack: people gasp for breath, worry that they are suffocating, and experience great
anxiety
  If had sudden intense arousal of SNS w/o knowing the reason, you might experience
it as an emotion
 Physiological responses seldom sufficient to produce emotional feelings, but they do
contribute
 Increases in heart rate intensify ratings of both pleasant and unpleasant emotions
 Some cortical areas that respond strongly to body’s autonomic responses also
respond strongly to emotional states
 Sensation caused by smiling increases happiness slightly
 Facial expression could alter emotions
o But smiles are not necessary for happiness
 Mobius syndrome cannot move facial muscles to smile but
experience happiness and amusement
 SO: our perceptions of the body’s actions contribute at least slightly to emotional feelings, as
the James-Lange theory proposed
 Emotions are embodied; they depend on responses of the body
 SO: SNS arousal neither necessary nor sufficient for an emotional experience but it
contributes to feeling aspect of emotion
o Is emotion a useful concept?
 Definitions of emotion include multiple aspects, such as cognition, feeling, and action
 But those aspects do not always stick tgt; can have one aspect along or two aspects
alone
 Perhaps emotion is not a coherent category
 Limbic system: forebrain areas surrounding the thalamus; regarded as critical for emotion;
amygdala + cerebral cortex react to emotional situations as well
 PET or fMRI to identify brain areas that respond while people look at emotional pictures
 Significant activation of a particular cortical area associated with happiness, sadness,
disgust, fear, or anger
o But variability of locations for each emotion
o But later found that no evidence for localization of emotions
 Shouldn’t expect scientific principle to explain what emotions really
are; socially constructed category that serves our purposes; does
not correspond to any category that exists in nature
 SO: no brain area is responsible for one and only one emotion
 Do people have a limited number of basic emotions?
o Emotion remains as the only area in which many researchers still hope to identify elements of
experience, to list a few basic emotions
o Basic emotions are the existence of facial expressions for happiness, sadness, fear, anger, disgust,
surprise, and etc.?
 Unconvincing
 Often see two or more emotions in a single face
 We also identify emotion by context and gestures in addition to facial expression
 Tone of voice and body posture as well
o If we find evidence for distinct basic emotions unconvincing, alternative view is that emotional
feelings vary along two or more continuous dimensions, such as weak/strong, pleasant/unpleasant,
or approach/avoid
 Behavioral activation system (BAS) = activity of left hemisphere especially frontal and
temporal lobes = marked by low to moderate autonomic arousal and a tendency to
approach, which could characterize happiness or anger
 Left hemisphere and approach; identify happy faces
 Behavioral inhibition system (BIS) = increased activity of frontal and temporal lobes of right
hemisphere; increases attention and arousal, inhibits action, and stimulates emotions such
as fear and disgust
 Right hemisphere and inhibition of action; identify sad/frightened faces
 The differences b/w the hemisphere relates to personality
 The functions of emotion
o Fear alerts us to escape from danger
 o Anger directs us to attack an intruder
o Disgust tells us to avoid sth that might cause illness
o Emotional expressions help us communicate our needs to others and understand other people’s
needs and probable actions
 Emotions provide us a useful guide when we need to make a quick decision
o Emotions and moral decisions
 When we make decisions, we pay attention to how we think an outcome will make us feel
 The trolley dilemma: kill five people or pull the switch to kill one person
 The footbridge dilemma: or push a stranger off the footbridge so trolley is blocked
 The lifeboat dilemma: push someone off the lifeboat because it’s starting to sink
 The hospital dilemma: kill the visitor and use the organs to save the five others
 In each of the dilemmas, you can save five people by killing one person
o Most people say it is right to pull the switch in the trolley dilemma, but
almost none agrees with killing one person to save five others in hospital
dilemma
o Contemplating the footbridge or lifeboat dilemma activates prefrontal
cortex and cingulate gyrus responsible for emotions
o More intense emotions when you imagine putting your hands on someone
rather than flipping a switch
 People with strongest autonomic arousal least likely to make the
logical decision to kill one and save five
 SO: when we make decisions about right or wrong, we seldom work it out rationally. One
decision or the other just feels right. After we have already decided, we try to think of a
logical justification
 SO: weaker autonomic arousal = stronger tendency to agree to push the person
o Decision making after brain damage that impairs emotions
 Damage to prefrontal cortex blunts people’s emotions, except for an occasional outburst of
anger
 Also impairs decision making
 Make impulsive decisions without pausing to consider consequences
 Make a quick decision and sigh or wince, knowing that they have made the wrong
choice
o These decisions are considered unemotional
o They make the utilitarian decision quickly and calmly for the dilemmas
mentioned above
 Phineas Gage with prefrontal cortex damage
 Impulsive behavior and poor decision making
 Antonio Damasio with prefrontal cortex damage
 Expressed almost no emotions
 Made bad decisions
 But knew the probable consequences of various decisions
o But did not anticipate that approval would feel good and trouble would feel
bad
o SO: any choice requires consideration of values and emotions
 Damage to a particular part of prefrontal cortex, ventromedial prefrontal cortex, people
show inconsistent preferences
 Deficient in sense of guilt
o In the one-shot Dictator game, they keep 90% of money
o In Trust game, give less, decreased trust or keep all the money instead of
returning it
 Show less than normal concern for others
 Failure to anticipate unpleasantness of likely outcomes leads to bad decisions
o Prefrontal cortex damage or amygdala (part of temporal lobe)
 True that emotions sometimes interfere with good decisions
 People with damage to prefrontal cortex do not panic in car
 Attack behaviors
o Vigorous emotional behaviors in animals and their corresponding emotions are closely related both
behaviorally and physiologically
o Attach behavior depends on the individual as well as the situation
 The home hamster attacks faster and more vigorously than first attack
 The first attack enhances its readiness to attack and gets it in the mood to fight
 Activity builds up in corticomedial area of amygdala and increases its probability of
attacking
 Counting ten before acting and lying on your back decrease anger
 SO: emotion is embodied – what you are doing affects how you feel
o Effects of hormones
 Most fighting in by animals is competing for mates by males or by defending their young by
females
 Male aggressive behavior depends on testosterone
o Highest in reproductive season
o Linked with increased striving for social dominance
 Men fight more often than women
 Those with higher testosterone levels tend to be more aggressive
o But the effects are small
 Because testosterone facilitates aggression whereas cortisol
(associated with fear and anxiety) inhibits aggression
 Aggression depends on the ratio of testosterone to cortisol, not
testosterone alone
 Serotonin also inhibits violent impulses
 SO: impulsive aggression is highest when testosterone levels are
high and both cortisol and serotonin are low
 Committees work more harmoniously if they include more women
o Serotonin synapses and aggressive behavior
 Nonhuman animals
 Isolating male mice increased aggressive behavior and decreased serotonin
turnover, the amount that neurons released and replaced
o When neurons release serotonin, they reabsorb most of it and synthesize
enough to replace the amount that washed away
o The amount present in neurons therefore remains fairly constant
o Measure turnover by [] of 5-hydroxyindoleacetic acid (5-HIAA), serotonin’s
main metabolite, in the CSF
 The more 5-HIAA, the more serotonin has been released and
presumably resynthesized
 SO: low serotonin turnover = more likely to get injured and die young due to
aggressiveness
o Why hasn’t natural selection eliminated the genes for low serotonin
turnover?
 1) evolution selects for an intermediate amount of aggression and
anxiety
 2) aggressiveness is a high-risk, high-payoff strategy
 Humans
 Low serotonin turnover in people = violent behavior
 But not a huge relationship
o SO: serotonin is evidently a contributor, but by itself not important to
enable us to make predictions
o Heredity and environment in violence
 Individual differences depend on both heredity and environment
 Violence tends to increase as weather grows hotter
 Exposure to lead, harmful to developing brains
o Decreased lead = declined violent crimes
 Monozygotic twins resemble each other more closely than dizygotic twins
o Genes influence violent behavior including autonomic arousal
  Low autonomic arousal = more aggressive = less strongly to fear of
consequences
 But no single or set of genes that will account for all variations in all
populations
 Enzyme monoamine oxidase A (MAOA)
 After a neuron releases serotonin, dopamine, or norepinephrine, most of it returns
to the neuron via reuptake
 At that point this enzyme breaks down some of it, preventing possible accumulation
of an excessive amount
 People vary in their genes for this enzyme
 Prediction: the more active form (low serotonin) = aggression
 But actually: low activity = aggression
o Depends on prior experience
 History of childhood maltreatment = less active MAOA = more
aggression
o The low activity of this gene is uncommon because it is an X-linked gene
 Far more men than women have low activity
 Greater prevalence of violent behavior in men
 Low serotonin activity is weakly associated with increased aggression, but the active form of
the MAOA gene that breaks down serotonin links to less aggression only for people with a
history of childhood maltreatment
 If we were to control human violence, biological interventions not the most
promising route

Neurobiology of emotional behaviors 2 (371-382, 475-486)

 Fear and anxiety

o Both experiences and genetics modify activity in amygdala regulating anxiety
o Role of the amygdala
 Moro reflex: a sudden loud noise causes a newborn to cry; built-in, unlearned fear
 Startle reflex: auditory info goes first to cochlear nucleus in the medulla and from there
directly to an area in the pons that commands tensing the muscles, especially the neck
muscles
 After infancy, a loud noise elicits this reflex
 Tensing neck muscles important cus neck is vulnerable to injury
 Very fast
 You don’t have to learn to fear loud noises, but current mood or situation modifies reaction
 If you are already tense, your startle reflex more vigorous
 Ppl with post-traumatic stress disorder (intense anxiety) show an enhanced startle
reflex
 SO: variations in startle reflex correlate well enough with anxiety that we can
measure the startle reflex to measure anxiety
o Can be used as a behavioral measure of anxiety = can use it with lab animals
to explore brain mechanisms as opposed to other types of emotion such as
happiness and anger
o Studies of rodents
 Animals learned to associate a stimulus with shock, that stimulus becomes a fear signal, and
presenting fear signal just before a sudden loud noise enhances startle response
 Amygdala important for enhancing startle reflex
 Cells in amygdala such as basolateral and central nuclei get input from pain fibers as
well as vision or hearing, so circuitry is well suited to establishing conditioned fears
 One path through amygdala responsible for fear of pain, another for fear of
predators, and another for fear of aggressive members of your own species
o Also controls changes in breathing, another controls avoidance of potentially
unsafe places, and another controls learning which particular places are
safest
 o The path from amygdala responsible for freezing in presence of danger is
separate from path controlling changes in heart rate
 Relevant to emotion cus what we call fear is a conglomerate of
separate aspects, not a single indivisible state
o Output from amygdala to hypothalamus controls autonomic fear responses,
such as increased blood pressure
 Also has axons to areas of prefrontal cortex that control approach
and avoidance responses
 Its axons to thalamus direct attention toward emotionally important
stimuli
 Can heighten responses of auditory cortex to a sound
associated with danger
 Additional axons extend from amygdala to midbrain areas that relay
info to pons and control startle reflex
 A rat with damage to amygdala still shows a normal startle reflex, but signals before
the noise do not modify the reflex, so no enhanced startle reflex after the light
o Ordinarily: present the stimulus before giving a loud noise; if the stimulus
increases startle reflex beyond its usual level, then the stimulus produced
fear
o Does it indicate amygdala damage destroys fear? No; maybe rats have
trouble interpreting stimuli with emotional consequences
o SO: The central amygdala receives sensory input from the lateral and
basolateral amygdala. It sends output to the central gray area of the
midbrain, which relays information to a nucleus in the pons responsible for
the startle reflex. Damage anywhere along the route from the amygdala to
the pons interferes with learned fears that modify the startle reflex
 Toxoplasma gondii = protozoan that infects many mammals but reproduces only in
cats
o Infected rats fearlessly approach a cat; amygdala damage
 Amygdala important for learning what to fear, but not the only type of fear
conditioning
o If attacked in a new place, become fearful in a wide variety of situations, not
only the stimulus
 Bed nucleus of the stria terminalis: long term, generalized
emotional arousal depends on this area; a set of axons that connect
this nucleus to amygdala; axons from this nucleus to ventral
tegmental area also control anxiety
 SO: damage to amygdala = startle reflex becomes consistent from one time or
situation to another
o Studies of monkeys
 Kluver-Bucy syndrome: amygdala damage in monkeys; tame and placid monkeys; pick up
lighted matches that they ordinarily avoid; display less fear of snakes or of larger dominant
monkeys; impaired social behaviors; impaired at learning what to fear
 Reactive amygdala = greatest fear in response to a noise
o Response of the human amygdala to visual stimuli
 Human amygdala reacts to photos that arouse fear (mainly), happiness or sadness, pleasant
stimuli
 Amygdala responds most strongly when a facial expression is a bit ambiguous or difficult to
interpret
 Recognize an angry expression faster if it’s directed toward you and a fearful
expression faster if it’s directed to side
 Amygdala responds most strongly to fearful face directed toward you
o Amygdala responds strongly to expression harder to interpret
o Individual differences in amygdala response and anxiety
 Infants with inhibited temperament => shy, fearful children and into shy adults who show an
enhanced amygdala response to sight of unfamiliar faces
  Part of variance in anxiety relates to genes controlling serotonin transporter (the protein
that produces reuptake of serotonin after its release)
 Ppl with genes for reduced serotonin reuptake tend to have increased responses to
threat and increased attention to threatening stimuli in social situations
o Anxiety disorders and difficult social interactions
o Married people with those genes more likely to react strongly to a marital
conflict
 Individual differences in anxiety correlate strongly with amygdala activity
 However, anxiety depends on more than just amygdala
 Cope with anxiety = reappraisal = reinterpreting a situation as less threatening
o Top-down influences from prefrontal cortex to inhibit activity in amygdala
 So people with depression = below-average activity in prefrontal
cortex
 Anxiety reactivity affects life even in political attitudes
 High support for military and police action = greater startle response to loud noises
 People with reactive amygdala react strongly to dangers so support strong
protection
 SO: amygdala responds more strongly to a fearful face directed at the viewer, rather than a
similar face looking to the side; easier to understand a fearful face looking to the side
 SO: people with highly reactive amygdala report many negative emotional responses, show
strong responses to stressful experiences, and favor strong reliance on military and police
power
o Damage to the human amygdala
 Continue to experience cognitive aspect of unpleasant emotions (can classify whether a
picture is pleasant or unpleasant), but much less of the feeling aspect (little arousal)
 Urbach-Wiethe disease: accumulate calcium in amygdala until it wastes away
 Extensive damage to amygdala w/o much damage to surrounding structures
 Impaired at processing emotional info and learning what to fear
o Fearlessness
 Feels angry, but not afraid
o The only thing that triggered fear in her was breathing in CO2 with a panic
attack; however, she agreed to do it again the following week
 Amygdala important for imagining fear or thinking about danger
 Fail to recognize emotional expressions in faces, especially of fear and disgust
 Trouble drawing a fearful expression
o Trouble identifying facial expressions of fear
o Why? Cus she looked at nose and mouth of each photograph
o Seldom made eye-contact
 Amygdala automatically directs attention toward emotionally significant stimuli
o Seeing the eyes important for recognizing fear
 Happiness with mouth, fear with eyes
 SO: Instead of amygdala being responsible for feeling fear or other
emotions, responsible for detecting emotional info and directing
other brain areas to pay attention to it in a proper way
 Anxiety disorders
o Increased anxiety = phobia and panic disorder
o Panic disorder: frequent periods of anxiety and occasional attacks of rapid breathing, increased
heart rate, sweating, and trembling; extreme arousal of SNS; more common in women and
adolescents and young adults
 Maybe genetic predisposition when looking at twin studies, but no single gene has been
identified
 Occurs in 15% of people with joint laxity (double jointed; able to bend fingers backward
farther)
 Even w/o panic disorder, stronger fears than most ppl
 Abnormalities in hypothalamus, not necessarily in amygdala
 Associated with decreased activity of NT GABA and increased orexin
 o Orexin = wakefulness and activity
o Drugs that block orexin receptors block panic responses
o Battle fatigue = shell shock = post-traumatic stress disorder (PTSD): frequent distressing flashbacks
and nightmares about the traumatic event, avoidance of reminders of it, vigorous reactions to noises
and other stimuli
 Cannot predict who will get PTSD based on the severity of trauma or intensity of person’s
initial reaction
 PTSD victims have a smaller than average hippocampus from the start, so that
increased the susceptibility to PTSD (cause, not an effect)
 Of those whose damage included amygdala, none suffered PTSD
 Of those with damage elsewhere in the brain, half suffered PTSD
 Amygdala, important for emotional processing, essential for extreme emotional impact that
produces PTSD
 Relief from anxiety (social support, reappraisal, exercise, distraction, gain a sense of control over the
situation)
o Pharmacological relief
 Orexin and CCK increase anxiety by their actions in amygdala and hippocampus
 Many drugs available to increase activity of GABA, inhibiting anxiety
 Anxiolytic (anti-anxiety) drugs are benzodiazepines, such as diazepam (Valium),
chlordiazepoxide (Librium), and alprazolam (Xanax)
 Benzodiazepines bind to GABAA receptor, which includes a site that binds GABA as
well as sites that modify sensitivity of GABA site
 At the center of GABAA receptors is a chloride channel
o When open, permits chloride ions to cross the membrane into neuron,
hyperbolizing the cell
o Surrounding chloride channel are four units, each containing one or more
sites sensitive to GABA
 Benzodiazepines bind to additional sites on three of those four units
 Neither opens nor closes the chloride channel but twists the
receptor so that GABA binds more easily
 Facilitate the effect of GABA
 Benzodiazepines exert anti-anxiety effects in the amygdala, hypothalamus, and midbrain
 Decreased learned shock-avoidance behaviors, relaxes muscles, increases social
approaches to other rats
 Decreases response in a rat’s brain to the smell of a cat
 Possibility of addiction
o When reached thalamus and cerebral cortex, induce sleepiness, block
epileptic convulsions, and impair memory
 Extremely stable chemically
o Alter resident fish
 No effect to a person w/o GABA
o Alcohol as an anxiety reducer
 Promotes flow of chloride ions through GABAA receptor complex by binding strongly at a
special site found on only certain GABAA receptors
 Ro15-4513 effective in blocking effects of alcohol on GABA receptors
 Blocks the effects of alcohol on motor coordination, its depressant action on brain,
and its ability to reduce anxiety
 Sobering-up pill? As a way to stop drinking alcohol? – too risky
o Learning to erase anxiety
 Anxiolytic drugs only temporary relief
 Systematic desensitization: expose you gradually to your feared object, in hopes of
extinction (in the classical conditioning sense)
 Relieve phobias with good success
 Virtual reality goggles
 However, extinction training dos not eliminate the original learning, only supresses it
– may reemerge in times of stress
  Easier to extinguish a learned response immediately after original learning than it is later
 After time has passed, learning becomes stronger = consolidated
 But not solid forever
 A memory reawakened by a reminder becomes labile – changeable (reconsolidated
or extinguished)
 If a similar experience follows the reminder, the memory is reconsolidated
o During the time when reconsolidation might occur, a well-timed extinction
experience can weaken the memory
 But depends on many details of procedure
o Decrease in fear correlates with a decreased response to the cue by the
amygdala
o Reconsolidation requires protein synthesis and altered synapses
 A drug intervention could facilitate extinction experience
 Propanolol interferes with protein synthesis at certain synapses in
the amygdala
 Blocks reconsolidation
o Much weaker emotional response to stimulus
 Major depressive disorder
o Major depression: feel sad and helpless most of the day every day for weeks at a time
 Changes in synapses to nucleus accumbens make it less responsive to reward
 Absence of happiness more reliable symptom than increased sadness
 Clinically significant depression = serious enough to warrant attention’
 More common in females, adults; if children, persists
 More common to have episodes of depression separated by periods of normal mood
 First episode special cus longer than most of the later episodes, and most patients
can identify a highly stressful event that triggered the first episode
o For later episodes, people are less and less likely to identify a triggering
event
 As if brain learns how to be depressed and gets better at it
 The more often you have had an episode, the easier it is to start
another one
o Genetics
 No one gene clearly important
 When we talk about depression, we may be combining separate syndromes
 People with early onset depression have a high probability of having other relatives
with depression as well as other psychological disorders
 People with late-onset depression have a high probability of relatives with
circulatory problems
 Certain genes link to depression only in people who have undergone severe stress
 Perhaps the effect of a gene varies with environment
 Gene that controls serotonin transporter, a protein that regulates ability of axons to
reabsorb serotonin after its release
o The short type and the long type
o With two short forms of the gene, increased numbers of stressful
experiences led to a major increase in the probability of depression
o With two long forms, stressful events slightly increased the risk of
depression
o With one long and one short, intermediate
o Short form of the gene by itself did not lead to depression, but it magnified
the reaction to stressful events
 But difficult to accurately measure either stress or depression
 In the absence of stressful experiences, the probability of becoming
depressed did not change
o Abnormalities of hemispheric dominance
 Strong relationship b/w happy mood and increased activity in left prefrontal cortex
  Ppl with depression have decreased activity in the left prefrontal cortex and increased
activity in the right prefrontal cortex = this imbalance is stable over years despite changes in
symptoms of depression = predisposition to depression
 Some people train you to use right hemisphere to increase creativity
 But predominant right-hemisphere activity and decreased left-hemisphere activity
show an increased tendency toward depression
 Antidepressant drugs
o Earliest psychiatric drugs discovered by accident
 Someone who noticed that workers in a rubber factory avoided alcohol traced the cause to
disulfiram, which altered the workers’ metabolism so they became ill after drinking alcohol
 Disulfiram = Antabuse
 Bromides sometimes relieve epilepsy
 Iproniazid (the first antidepressant drug) was originally marketed to treat tuberculosis but
relieved depression
 Chlorpromazine alleviates schizophrenia
 In the past, evaluated the new drugs by trial and error; now, use test tubes or tissue samples
and then lab animals
o Types of antidepressants
 Tricyclics, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, and
atypical antidepressants
 Tricyclics (imipramine, Tofranil) operate by blocking the transporter proteins that reabsorb
serotonin, dopamine, and norepinephrine into presynaptic neuron after their release
 Serotonin transporter protein picks up a serotonin molecule outside the membrane
and then flips into position to deliver the molecule to the inside of the neuron
o A tricyclic drug locks the transporter into the initial position
o As a result, prolong the presence of the NTs in the synaptic cleft, where they
continue stimulating the postsynaptic cell
o Also block histamine receptors (side effects: drowsiness), acetylcholine
receptors (dry mouth and difficulty urinating), and certain sodium channels
(heart irregularities)
o SO: Tricyclic drugs block reuptake of serotonin and catecholamines. They
also block histamine receptors, acetylcholine receptors, and certain sodium
channels, thereby producing unpleasant side effects
 Selective serotonin reuptake inhibitors (SSRIs): similar to tricyclics but specific to NT
serotonin
 Fluoxetine (Prozac): blocks reuptake of serotonin
 Produce milder side effects than tricyclics, but same effectiveness
 Sertraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa), and paroxetine (Paxil or
Seroxat)
 Serotonin norepinephrine reuptake inhibitors (SNRIs): duloxetine (Cymbalta) and
venlafaxine (Effexor) block reuptake of serotonin and norepinephrine
 Monoamine oxidase inhibitors (MAOIs): (e.g., phenelzine, trade name Nardil) block the
enzyme monoamine oxidase (MAO), a presynaptic enzyme that metabolizes catecholamines
and serotonin into inactive forms
 When they block this enzyme, presynaptic terminal has more of its transmitter
available for release
 Earliest antidepressants
 First try with tricyclics or SSRIs first and try MAOIs later
o If treating with MAOIs, must avoid foods containing tyramine (cheese,
raisins) cus increase blood pressure
o SO: MAOIs block the enzyme MAO, which breaks down catecholamines and
serotonin. The result is increased availability of these transmitters
 Atypical antidepressants: bupropion (Wellbutrin) which inhibits reuptake of dopamine and
to some extent norepinephrine but not serotonin
  Ketamine, which antagonizes NMDA type glutamate receptors and also increases
formation of new synapses, produce rapid antidepressant effects in patients who
don’t respond to other medications
o Also sometimes produce hallucinations and delusions
 L-acetylcarnitine, which produces epigenetic changes on glutamate receptors
o Rapid antidepressant results with few side effects
 St. John’s wort (an herb) = antidepressant
o Nutritional supplement; less expensive; available w/o prescription
o Decreases effectiveness of other drugs you might be taking
 Increases the effectiveness of the liver enzyme responsible for
breaking down plant toxins
o Why are antidepressants effective?
 Increasing levels of NTs at synapses NOT sufficient to explain benefits of the drugs
 Neurotrophins aid in survival, growth, and connections of neurons
 Ppl with depression have lower level of neurotrophin called brain-derived
neurotrophic factor (BDNF) that is important for synaptic plasticity, learning, and
proliferation of new neurons in the hippocampus
o Low BDNF = smaller hippocampus, impaired learning, and reduced
production of new hippocampal neurons
o Antidepressants increase BDNF levels
 Conflicting
 But proliferation of new neurons in hippocampus appears to be
important for antidepressant effects, regardless of whether BDNF is
responsible for that proliferation
 Procedures that block neuron production also block behavioral
benefits of antidepressant drugs
 Capacity to make new neurons makes it easier to learn new ways of
coping
 Importance of new learning = antidepressants do not elevate mood
of people who are not depressed = they aren’t burdened with
discouraging thoughts that they need to unlearn
 SO: normal mood person do not feel better with antidepressant
drugs because the drugs promote new learning that competes with
depressed thoughts; someone without depressed thoughts has little
gain
 SO: time course of antidepressants conflicts with the idea that they improve mood by
increasing NT levels
 Antidepressants produce their effects on serotonin and other NTs quickly, but their
behavioral benefits develop gradually over 2 to 3 weeks
 SO: as opposed to an interpretation in terms of NT levels, the alternative explanation for the
benefits of antidepressant drugs
 They increase production of BDNF, which promotes growth of new neurons in
hippocampus and new learning
 SO: switching between two drugs and showing improvement after does not make any
conclusion
o How effective are antidepressants?
 Trial and error process
 Switching to a different type of drug is no more likely to be helpful than switching to
a drug of the same type
 Hamilton Depression Rating Scale = higher scores = intense depression
o Many responded well on placebos
o Only for people with severe depression did the drugs show a meaningful
advantage = not sure
 But antidepressant drugs are only moderately helpful for most
patients with depression, and not helpful at all for many of them
o Alternatives to antidepressant drugs
  Cognitive-behavioral therapy
 Antidepressant drugs and psychotherapy are about equally effective for treating
depression
 Antidepressants and psychotherapy increase metabolism in the same brain areas
o If mental activity is the same thing as brain activity, then changing
someone’s thoughts should indeed change brain chemistry (monism)
 Psychotherapy has an advantage because its effects are more likely to last
o Relapse into depression is more likely after antidepressant drug treatment
than after psychotherapy
 People receive both treatments show slightly greater improvement than people
receiving either one alone
 SO: for more severe cases of depression, percentage of patients who improve
remains about the same for patients taking antidepressant drugs, but fewer patients
taking placebos show improvement
 SO: psychotherapy and antidepressant drugs help about an equal percentage of
patients and mostly the same patients
 SO: people who respond well to psychotherapy have a lower risk of later relapse
than people who respond to antidepressant drugs, which produce unpleasant side
effects
 Exercise
 The simplest, least expensive antidepressant treatment
 Modest antidepressant benefits
 Exercise increases brain levels of serotonin and BDNF and that it increases sensitivity
to reward
 Electroconvulsive therapy (ECT): benefits don’t last long
 For people with both epilepsy and schizophrenia, when symptoms of one disorder
increase, symptoms of the other often decrease
 Insulin shock: dreadful experience
 Quick, most patients awaken calmly w/o remembering it
 ECT did relieve depression in many cases
o Use ECT for patients with severe depression who have not responded to
antidepressant drugs
 Side effect: memory impairment; but limiting the shock to the right hemisphere
reduces the memory loss
o Quick and fast recovery/benefits but high risk of relapse
 ECT increases proliferation of new neurons in hippocampus
o Alters expression of 120 genes in hippocampus and frontal cortex
 Similar treatment = transcranial magnetic stimulation for depression
 Altered sleep patterns
 Ppl with depression have sleep problems = mood changes
 Usual sleep pattern for a person with depression resembles the sleep of healthy
people who travel a couple time zones west and have to go to bed later than usual
o Depressed people have their circadian rhythms advanced
 Sleep as if they had gone to bed later than they actually did
o Sleep deprivation + antidepressant drugs = helpful
o Sleep deprivation causes astrocytes to release adenosine, which has
antidepressant effects
o Go to bed earlier than usual and wake up earlier than usual!
 Deep brain stimulation
 Physician implants a battery-powered device into brain to deliver periodic
stimulation to certain brain areas
 Optogenetic stimulation: control individual connections rather than all the axons
going from one area to another
 Bipolar disorder
o Depression can be either unipolar or bipolar
 Unipolar disorder: vary b/w normality and depression
  Bipolar disorder: manic-depressive disorder; alternate between two poles; depression and
mania
 Mania: restless activity, excitement, laughter, excessive self-confidence, rambling
speech, and loss of inhibitions
o Bipolar I disorder: full-fledged manic episodes
o Bipolar II disorder: mild or hypomanic episodes
o Men are more likely to have bipolar I case, but women are more likely to get
treatment
o Brain’s increase in glucose use during mania and decrease during depression
 Has been linked to many genes, but none of them are specific
 The same genes increase the risk of unipolar depression,
schizophrenia, etc.
o Treatments
 Lithium salts to treat bipolar disorder
 Stabilize mood, preventing a relapse into either mania or depression
 E.g., valproate and carbamazepine
 Antidepressant drugs are risky, provoking a switch from depression to mania
 Antipsychotic drugs are helpful but produce unpleasant side effects
 They all decrease the number of AMPA type glutamate receptors in hippocampus
o Excessive glutamate activity = mania
o Drugs that are effective against bipolar disorder block synthesis of a brain
chemical called arachidonic acid, produced during brain inflammation
o Bipolar patients = increased expression of genes associated with
inflammation
 Counteracted by omega-3 fatty acids in seafood contained in
arachidonic acid
 Sleep
o Patients get little sleep during manic phase; variable sleep during depressed
phase
o Sleep disturbance = warning sign of renewed episode of mania or
depression
o Getting consistent, adequate sleep stabilizes mood and decreases risk of a
new episode
 Seasonal affective disorder
o Seasonal affective disorder (SAD): depression that recurs during a particular season, such as winter
 most prevalent near the poles, where winter nights are long
 phase-delayed sleep and temperature rhythms
 phase-advanced = depression
 seldom as severe as major depression
 mutation in one of the genes responsible for regulating circadian rhythm
 Bright light = cheaper, no side effects, quick benefits
Neurobiology of cognitive functions 1 (423-447)
 Language, though, and attention (cognition) hard to measure and study
o Damage to corpus callosum: two fields of awareness
o Damage to left hemisphere: lose language abilities
o Damage to right hemisphere: ignore the left side of body and left side of world
o Human brain is asymmetrical; different functions in two hemispheres give advantages
 The left and right hemispheres
o Left hemisphere of cerebral cortex connects to skin receptors and muscles on the right side of body,
and vice versa
 Both hemispheres control trunk muscles and facial muscles
 Left hemisphere sees right half of the world, and vice versa
 Each hemisphere gets auditory info from both ears but slightly stronger info from
contralateral ear
 Animals too
 Taste and smell uncrossed, not contralateral
 Taste from both sides of tongue
 Smell from the nostril on its own side
 Corpus callosum: left and right hemispheres exchange info through this set of axons and
through anterior commissure + hippocampal commissure + other small commissures
 Two hemispheres are not mirror images
o Left hemisphere = language
o Right hemisphere = difficult to summarize
 Lateralization: division of labor between the two hemispheres
o If no corpus callosum, left hemisphere react only to info from right side of
body and vice versa
o But because of corpus callosum, each hemisphere receives info from both
sides
 Only after damage to it we see clear evidence of lateralization
 Visual and auditory connections to the hemispheres
o Hemispheres connect to eyes such that each hemisphere gets input from opposite half of the visual
world
 Left hemisphere sees right side of the world and vice versa
 Rabbits and other animals with eyes far to the side of the head
 Not for humans
o You see left side of the world almost as well with your right eye as with your
left eye
o Light from the right half of the visual field (what is visible at any moment)
strikes the left half of each retina, and light from left visual field strikes the
right half of each retina
 Left half of each retina connects to the left hemisphere, so see right
visual field and vice versa
 A small vertical strip down the center of each retina, covering 5
degrees of visual arc, connects to both hemispheres
 Half of the axons from each eye cross to the opposite side of the
brain at the optic chiasm
 SO: right visual field = left half of each retina = left hemisphere
 Left visual field = right half of each retina = right hemisphere
 At the optic chiasm, those from nasal (inside) half of each
retina cross to the opposite hemispheres
 SO: left hemisphere of brain connected to right eye in guinea pigs; in
humans, left hemisphere connected to left half of each retina
  Right eye far to the side of head and sees only right visual
field in guinea pigs; eyes point straight ahead and half of
each sees right visual field in humans
o Each ear sends info to both sides of brain because any brain area that contributes to localizing
sounds must compare input from both ears
 However, each hemisphere does pay more attention to the ear on the opposite side
 The corpus callosum and the split-brain operation
o Damage to it prevents the hemispheres from exchanging info
o Epilepsy: repeated episodes of excessive synchronized neural activity
 Sever corpus callosum as a treatment
 The disorder can result from a mutation in a gene controlling GABA receptors, from trauma
or infection in brain, brain tumors, or exposure to toxic substances
 Antiepileptic drugs block sodium flow across membrane or enhance effects of GABA
 If someone continues having frequent seizures despite medication, surgically remove focus,
the point in brain where seizures begin
 Not an option if having several foci, or if the focus is in an area considered essential
for language
o So cut corpus callosum to prevent epileptic seizures
 Benefit: epileptic seizures affect only half of the body + seizures
become less frequent
 Seldom performed today
o Severing corpus callosum affects other aspects of behavior
 Ppl undergone the surgery = split-brain people maintain intellect and motivation and walk
w/o difficulty, use two hands tgt, do well on well-practiced tasks
 But struggle on unfamiliar tasks
 Can use their two hands independently in a way that other cannot
o So for normal ppl, cognitive difficulty rather than motor difficulty
o Split-brain ppl have no trouble planning different actions with two hands
 However, if the left hemisphere concentrating on a difficult task, the
drawings or other activities by the right hemisphere and left hand
deteriorate
 Two hemispheres do not work entirely independently
o Left hemisphere dominant for speech production in more right handers; left handers variable (from
the start)
 But language comprehension equally divided
 The left hemisphere understands speech better than the right hemisphere, but the right
hemisphere can generally understand speech if the vocabulary and grammar are relatively
simple; Therefore, an investigator can give instructions to both hemi- spheres of a split-brain
person, but only the left hemisphere can reply vocally.
 The word hatband: a person with a split-brain reports only what her left hemisphere saw,
band; with left hand, point to a hat, which is what the right hemisphere saw
 Some split-brain ppl get enough info to give a partial description of what the right
hemisphere saw due to having small commissures
o Advantage for just one hemisphere to control speech?
 Perhaps; a conflict between two speech centers produces
competing messages to speech muscles
 SO: A split-brain person can draw different things with the two
hands at the same time, or move the hands at different speeds at
the same time
 SO: A split-brain person can describe something after feeling it with
the right hand but not with the left. The right hand sends its
information to the left hemisphere, which is dominant for language
in most people. The left hand sends its information to the right
hemisphere, which cannot speak
o Split hemispheres: competition and cooperation
  In the first weeks after the surgery, the hemispheres act like separate people sharing one
body
 But over time it gets better because brain learns to use smaller connections between
the hemispheres
o The left hemisphere somehow suppresses the right hemisphere’s
interference and takes control in most situations
 Cooperation: Suppose an experimenter flashes a picture in the left visual field and asks,
“Was it green?” The left (speaking) hemisphere takes a guess: “Yes.” That guess might be
correct. If not, the right hemisphere, knowing the correct answer, makes the face frown.
(Both hemispheres control facial muscles on both sides of the face.) The left hemisphere,
feeling the frown, says, “Oh, I’m sorry, I meant ‘no.’
 With right hand, drew what he had seen in right visual field (left hemisphere)
 With left hand, drew literal combination of two words, such as overheated dog for
hot and dog
o Through the bilateral mechanisms of medial corticospinal pathway, left
hemisphere can move the left hand clumsily and add what it saw in the right
visual field
 When right hemisphere does sth, left hemisphere doesn’t know why
o Invents an explanation
 Interpreter: tendency of left hemisphere to invent and defend
explanations for actions even when the true causes are unconscious
o The right hemisphere
 Comprehend spatial relationships
 Left hemisphere focuses on details; right hemisphere more on overall patterns
 w/o help of right hemisphere, the left hemisphere’s understanding is sometimes
overly literal
 More responsive to emotional stimuli than the left
 Better at perceiving emotions in people’s gestures and tone of voice
 Split-brain people have the right hemisphere that does better at recognizing
whether two photographs show same or different emotions
o What you see in your left visual field stimulates your right hemisphere first
 A procedure in which one hemisphere at a time was anesthetized by drug injection into one
of the carotid arteries, which provide blood to the head
 Wada procedure, used for kinds of brain surgery
o When right hemisphere inactive, do not experience strong emotions and do
not remember feeling them
o Hemispheric specializations in intact brains
 More difficult to do two things at once when both activities depend on the same hemisphere
 Left hemisphere: speech; right hemisphere: emotional inflection of speech, interpreting
others’ emotional expressions, and spatial relationships
 Development of lateralization and handedness
o Anatomical differences between the hemisphere
 One section of temporal cortex, planum templorale, is larger in left hemisphere for 65% of
people
 So hemispheres differ from the start
 Chimpanzees with a larger left than right planum temporale show a preference for
using right hand
o Similar to humans; built-on specializations in ancestors
o Maturation of the corpus callosum
 It gradually grows and thickens as myelin increases around axons during childhood and
adolescence
 Matures by discarding many axons
 A neuron in left hemisphere that responds to light in the center of fovea should be
connected to a right-hemisphere neuron that responds to light in same location
  Therefore, many connections form across the corpus callosum, but only those axons
that connect cells with similar functions survive
 Connections take years to develop; children show similar behaviors as split-brain patients
 Corpus callosum immature in 3-year-olds
o When asked to compare fabrics that they feel with one hand or two, 3-year-
olds are much more accurate with one hand. The interpretation is that
immaturity of the corpus callosum makes it difficult for these children to
compare input from the two sides of the body
 Avoiding overstatements
o I am not good at science cus it’s a left-brain subject
 The scientific ideas are that (1) the hemispheres are specialized for different functions, and
(2) certain tasks evoke greater activity in one hemisphere or the other. The doubtful premise
is that any individual habitually relies mostly on one hemisphere
 Right-brained: do well on creative tasks and do poorly on logical tasks
o But difficult tasks require cooperation of both hemispheres
 Evolution and physiology of language
o Nonhuman animals do communicate thru visual, auditory, tactile, or chemical (pheromonal)
displays, but those signals do not have much flexibility
o Human language stands out cus of productivity, ability to improvise new combo of signals to
represent new ideas
 Nonhuman precursors of language
o Common chimpanzees
 Attempts to teach chimpanzees to talk failed
 Humans vocalize while breathing out, whereas chimpanzees vocalize while
breathing in
 However, chimps communicate with gestures
 They learned to press keys bearing symbols to type messages on a computer
o But: 1) they seldom used symbols in a new, original combo; their symbol use
was short on productivity 2) they used symbols mainly to request, seldom to
describe
o Bonobos
 Males and females form strong, some- times lasting, personal attachments. They often
copulate face to face. The female is sexually responsive on almost any day and not just
during her fertile period. The males contribute significantly to infant care. Adults often share
food. They stand comfortably on their hind legs. In short, they resemble humans more than
other primates do
 Explanations 1) bonobos more language potential than common chimps 2) but
bonobos began language training when young 3) learning by observation and
imitation promotes better language understanding than formal training methods of
previous studies
o Nonprimates
 Parrots kinda successful
 Through nonhuman studies, gain insights into how best to teach language to brain damaged
people or children with autism; indicate that human language evolved from precursors
present in other species; also, we cannot decide the chimps or parrots have language unless
we define language more precisely
 How did humans evolve language?
o An important step toward vocal communication = phonological loop = ability to hear sth and
remember it
 Humans have stronger connections b/w auditory cortex and prefrontal cortex, enabling
greater auditory memory
 Auditory working memory not sufficient but necessary
o Maybe it evolved from communication by gestures
 Mouth gestures as well
  With regard to brain, what changed to make language possible? 1) we evolved it as a by-
product of overall brain development or 2) we evolved it as a specialization
o Language: by-product of intelligence (brain size), or specialized adaptation?
 First hypothesis faces problems = whales and dolphins have larger brains than us but no
language
 People with normal intelligence but impaired language
 If language is a product of overall brain size, then anyone with a full-sized brain and
normal overall intelligence should have normal language. However, not all do
 So language requires more than just a large brain and overall intelligence
 People with relatively spared language but low overall intelligence; the reverse
 Williams syndrome: poor at tasks related to numbers, visuomotor skills (copying a
drawing), and spatial perception (finding way home), lapses of attention, poor
planning, and difficulty inhibiting inappropriate responses
 But speak fluently
o Cause of the disorder: deletion of several genes from chromosome 7,
leading to decreased gray matter in visual processing areas
o But do not handle language perfectly
 In short, language is not simply a by-product of overall intelligence
 Language as a specialization
 Language acquisition device: a built-in mechanism for acquiring language
o Most children develop language so quickly and easily that it seems they
must have been biologically prepared for this learning. Also, deaf children
quickly learn sign language, and if no one teaches them a sign language, they
invent one and teach it to one another
 Trouble with pronunciation and basic grammar: mutation in a gene designated
FOXP2, which regulates a protein that promotes synapse formation in cerebral
cortex
o Both humans and chimps have this gene, but differs in two places, resulting
in proteins with different amino acids
 Produce effects on brain development and on structures of jaw and
throat important for speech
 One speculation is that language relates to the long period of dependency in
childhood. Social interactions among people favored the evolution of language. In
that case, overall intelligence may be a by-product of language development more
than language is a by-product of intelligence
 SO: language evolution depended on overall evolution of brain and intelligence =
some people have normal brain size but very poor language. Also, some people are
mentally retarded but nevertheless develop nearly normal language
 SO: Williams syndrome: Poor: self-care skills, attention, planning, numbers, visual-
motor skills, and spatial perception. Relatively good: language, interpretation of
facial expressions, some aspects of music
o A sensitive period for language learning
 People who grow up in a bilingual home, speaking 2 languages from the start, show bilateral
activity during speech, for both language
 But just the left hemisphere if learned a language after age 6
 Bilingual takes extra effort to find the right word and inhibit the incorrect word cus
activate larger area of brain
o But can shift attention back and forth with ease
 Important to learn language in early childhood
o Deaf children not exposed to sign language until later in life do not become
proficient at it
 Brain damage and language
o Broca’s aphasia (nonfluent aphasia)
  Aphasia (language impairment) in Broca’s area = damage in left frontal cortex
 When brain damage impairs language production = Broca’s aphasia or nonfluent
aphasia
 Damage to only Broca’s area produce only minor language impairment
o Got to be much of left hemisphere
 Most cases of Broca’s aphasia related to combined damage to parts of cortex,
thalamus, and basal ganglia
 Impaired language production
 Slow and awkward with all forms of language communication, including speaking,
writing, and gesturing, and sign language as well
 Meaningful speech but sparse
 Omit grammatical words and endings if speaking English
 More word endings for German and Italian
 Seldom use closed-class words (prepositions, helping verbs, conjunctions)
 Omit grammatical words and endings
 Problems in comprehending grammatical words and devices
 People with Broca’s aphasia understand most speech, except when the meaning
depends on prepositions, word endings, or complex grammar—the same items that
they omit when speaking
 But have not totally lost their knowledge of grammar; recognize sth is wrong in
sentence but don’t know how to improve it
 SO: They have the greatest trouble with “closed-class” words that are meaningful
only in the context of a sentence, such as prepositions, conjunctions, and helping
verbs. They have the most trouble understanding the same kind of words they have
trouble producing— the closed-class words
o Wernicke’s Aphasia (Fluent Aphasia)
 Damage to left temporal cortex near auditory cortex = poor language comprehension and
impaired ability to remember the names of objects
 Fluent aphasia cus still can speak smoothly
 1) articulate speech 2) difficulty finding the right word; anomia: difficulty recalling names of
objects 3) poor language comprehension – its recovery correlated with increased blood flow
to Wernicke’s area
 Although Wernicke’s area and surrounding areas are important, language comprehension
also depends on the connections to other brain areas. For example, reading the word lick
activates not only Wernicke’s area but also the part of the motor cortex responsible for
tongue movements. Reading throw activates the part of the premotor cortex controlling
hand movements
 SO: People with Wernicke’s aphasia speak fluently and grammatically but omit most nouns
and verbs and therefore make little sense. 14. People with Wernicke’s aphasia understand
little speech.
 Type; Pronunciation; Content of speech; Comprehension
o Broca’s aphasia; poor; mostly nouns and verbs + omits prepositions and other grammatical
connectives; impaired if meaning depends on complex gramma
o Wernicke’s aphasia; unimpaired; grammatical but often nonsensical + has trouble finding the right
word, especially names of objects; seriously impaired
 Music and language
o Both evoke strong emotions and rely on detecting small changes in sound
o Sight-reading music strongly activates Broca’s area
o Use the language areas of the brain when composing music
o Musical composition tends to follow the same rhythms that are common in the language spoken by
the composer
 Dyslexia: specific impairment of reading in someone with adequate vision, motivation, cognitive skills, and
educational opportunity
o More common in boys and in English
 Cus English has many words with irregular, nonphonetic spellings
 o Occurs in all languages and always pertains to a difficulty converting symbols into sounds
o More likely to have a bilaterally symmetrical cerebral cortex, whereas in other people, the planum
temporale is larger in left hemisphere
 Parietal and temporal cortex have less gray matter in children with dyslexia, show less
arousal during reading
o When compared brains of dyslexic readers and normal readers some of differences are causes of
poor reading and some are results of less practice at reading
o Different ppl have different kinds of reading problems, so no one explanation for all
 Most have auditory problems; some have impaired control of eye movements; some have
both
 Ability to hear sth is most seriously impaired in dyslexia
o Dysphonetic dyslexics have trouble sounding out words, so memorize each word as a whole
o Dyseidetic readers sound out words well, but fail to recognize a word as a whole; read slowly and
have particular trouble with irregularly spelled words
o Problem with how the brain handles auditory info, not a problem with the auditory info itself; poor
auditory memory; weaker connections b/w auditory cortex and Broca’s area
o Trouble detecting temporal order of sounds and making Spoonerisms (Trading first consonants of
two words)
o Abnormalities in attention
 Treatment: teach them to attend to just one word at a time
 Twist: they would rather return to being dyslexic cus multitasking possible
 Their reading skills were overall tied to attentional strategies

Neurobiology of cognitive functions 2 (448-458)

 The mind-brain relationship
o Mind-body or mind-brain problem: what is the relationship between the mind and the brain?
 most widespread view among non-scientists: dualism, belief that mind and body are
different kinds of substance that exist independently
 both mind and brain interact at a single point in space, at the pineal gland
 Nearly all reject dualism cus dualism contradicts the law of the conservation of
matter and energy. According to that law, the only way to influence matter and
energy, including that of your body, is to act on it with other matter and energy
o According to dualism, a mind that is not composed of matter or energy
cannot make anything happen, like muscle movements
 Monism: the belief that universe consists of only one kind of substance
 Materialism: the view that everything that exists is material, or physical
 Mentalism: the view that only minds really exist and that the physical world could
not exist unless some mind were aware of it
 Identity position: view that mental processes and certain kinds of brain processes
are the same thing, described in different terms
o Says that mental activity (mind) = brain activity, not just brain
 Monism is the most reasonable working hypothesis
o Cannot have mental activity w/o brain activity and cannot have brain activity
w/o mental activity
 Easy problem of consciousness: difference b/w wakefulness and sleep and what brain
activity occurs during consciousness
 Hard problem of consciousness: why consciousness exists at all
 Consciousness of a stimulus
o Main difficulty: we cannot observe consciousness
 Defining is difficult too
 Operational definition: if a cooperative person reports awareness of one stimulus and not
another, then he or she was conscious of the first and not the second
 But with individuals who cannot speak, this doesn’t apply
 Flash suppression: strong response to the flashing stimulus decreases the responses to the
steady stimulus, as if it were a fainter light
 o Experiments using masking
 Masking: a brief visual stimulus is preceded and followed by longer interfering stimuli
 Backward masking: presenting brief stimulus and a final, longer stimulus
 In the masking condition, they say they saw no word at all
o The conscious and unconscious stimuli were physically the same, but the
difference was that a stimulus did not become conscious if it was preceded
and followed by an interfering pattern
o Using fMRI and evoked potentials, they found that stimulus initially activates
primary visual cortex in both conscious and unconscious conditions but
activates it more strongly in conscious condition
 Additionally activates prefrontal cortex and parietal cortex in
conscious condition
 A conscious stimulus also synchronizes responses for
neurons in various brain areas (gamma waves)
o Synchronized action potentials = their synaptic
inputs arrive simultaneously at target cells =
maximal summation
 SO: consciousness of a stimulus depends on amount and
spread of brain activity
o Experiments using binocular rivalry
 Binocular rivalry: seeing sth requires seeing where it is, and brain cannot perceive both
patterns in the same location so your perception alternates
 some see with one eye longer than the other
 Emotionally charged image holds attention longer than a neutral image
 Each shift in perception accompanies by a shift in activity over a large portion of
brain
 A conscious stimulus strongly activates much of brain, taking over brain activity
o When stimulus unconscious, produces weaker and less widespread activity
o Flash suppression, backward masking, and binocular rivalry = to find out what happens in brain
during consciousness
o The fate of an unattended stimulus
 A meaningful stimulus captures attention faster than a meaningless stimulus; like your name
and your first language words
 SO: much of brain activity is unconscious, and even unconscious activity can
influence behavior
 SO: use fMRI to determine which of two patterns in binocular rivalry is conscious at a
given moment: Make one stimulus pulsate at a given rhythm and look for brain
areas showing that rhythm of activity. The rhythm takes over widespread areas of
the brain when that pattern is conscious.
 SO: if someone aware of stimulus on the right in case of binocular rivalry, what
evidence says that brain is also processing the stimulus on the left?
o If a stimulus gradually appears on the left side, attention shifts to the left
faster if that stimulus is a meaningful word than if it is a word from an
unfamiliar language.
o Consciousness as a threshold phenomenon
 Consciousness is a yes-no phenomenon = threshold phenomenon = all-or-none
phenomenon
o The timing of consciousness
 Phi phenomenon: if you see a dot in one position alternating with a similar dot nearby, it’ll
seem that the dot is moving back and forth
 the second position changed your perception of what occurred before it
 so you are capable of becoming conscious of sth after it is gone
o your brain held it in reserve, capable of activating it after the fact
 intermediate duration of presentation: people are sometimes conscious of it and sometimes
not, and stimuli after the event can influence the outcome
 Conscious and unconscious people
 o Loss of consciousness marked by decreased overall activity and decreased connectivity b/w cerebral
cortex, subcortical areas such as thalamus, hypothalamus, and basal ganglia
 Regained connectivity when recovered
o Some people in a vegetative state used brain activity when asked questions
 More widely spread brain activity in people in a minimally conscious state
 Attention
o Isn’t synonymous with consciousness but is closely related
 Can be conscious w/o paying attention but cannot pay attention w/o being conscious
 For humans only
 Inattentional blindness or changed blindness: conscious of only those few to you direct
attention
o Brain areas controlling attention
 Bottom-up process depends on stimulus
 E.g., a running dear
 Top-down process is intentional
 E.g., looking for someone in the crowd
 Sometimes overrules bottom-up
 Depends on prefrontal cortex and parietal cortex
 Can control your top-down attention even w/o moving eyes
o But increase activity of visual cortex
 When you direct attention to left foot that you weren’t conscious of before,
somatosensory cortex activity increased
 Stroop effect: difficulty of ignoring words and saying the color of ink
 Enhance activity in color-vision areas of the cortex and decrease activity in areas
responsible for identifying words
 On trials when activity was enhanced in the middle frontal gyrus (part of prefrontal
cortex) at the start of the trial (before seeing the stimuli) people did best at ignoring
red square and resist distraction
o Importance of prefrontal cortex in directing attention
 Ppl who habitually play action video games do better on an attention tests cus
enhanced top-down control
o Intensive training at meditation also improves attention
o Spatial neglect: damage to right hemisphere; a tendency to ignore the left side of the body, left side
of objects, what they hear in left hear, what they feel in left hand
 Put clothes on only the right side of the body
 Damage in left hemisphere seldom produces significant neglect of right side
 Hard time choosing the center of a long line
 Most people rate and find the centre of a long line slightly left
 Main problem is loss of attention in the left side rather than impaired sensation
 Saw the H’s comprising the big E but when asked to cross out all the H’s, only did on
the right side cus didn’t pay attention to the left side
 Someone who neglects left hand pays attention to it when it’s crossed over the right
hand
 See the forest but only half the trees
 Treatment: Simply tellingthe person to attend to something on the left helps
temporarily. Having the person look to the left while feeling something on the left
side increases attention to the felt object. Crossing the left hand over the right
increases attention to the left hand. Moving a hand far to the left makes it easier for
the person to point to something in the left visual field because the hand will move
toward the right to point at the object