A Brief History of Mood Disorder

1. Describe 5 historical figures and propose their diagnosis of mood disorder based on their beliefs.
a. Hippocrates believed that mood disorders stem from physiological imbalances of our elements known as fluids.
He proposed that by looking at the color of our bodily fluids, we can determine the mood experienced by the individual.
These include:
i. Cholericà yellow bile
ii. melancholicà black bile
iii. sanguineà blood
iv. phlegmaticà phlegm
b. Pythagoras, like Hippocrates, also relied on this naturalistic approach to mood disorders as he described how
our biological humors determined our mood. Such humors were based on impulse (genital area), intelligence (heart), and
reason (brain).
c. Confucius also believed that physiological imbalances were causing illness. In the context of mood disorder, it
would be a result of the imbalance of the 5 elements of wood, water, fire, metal, earth and fire.
d. Socrates would deduce our cause of mood disorders based on how strong our mentality of reason/intelligence
was in terms of our animalistic urges. The stronger the animalistic urge was, the stronger the mood disorder. The way to
treat mood disorders would be to overcome such urges with thought and reason
e. Aristotle believed that our bodily temperature had control of our mood; the hotter the more mood disorder we
experienced. Aristotle’s Heart was a study conducted by the man himself in which determined that the heart, being the
hottest organ in the body (due to its activeness) is the source of thought and emotion.

2. Describe 3 historical events that influenced our understanding of mood disorders.

a. Inquisition of the 13th Centuryà there was an influx of fungus on wheat. People would eat the wheat (whether
in bread), and begin to hallucinate. The paranoia of the growing incidence of cases led to speculate that the devil was
coming; thus beginning the inquisition. Many who suffered from hallucinations were thought to be influenced by the devil
and therefore were targeted for killing.
b. The Plague 14th Centuryà During the plague, the 1st madhouse was built for the mentally ill at St. Mary of
Bethlehem in 1247. Casualties from the death were thought to be the mentally ill.

3. Evaluate ways that historical misconceptions still influence our beliefs about mental illness.
Historical misconceptions still influence our beliefs of mental illness as they prevent us from seeking treatment. It
leads to stigmatization of the illness as it places blame on the individual when structural and social factors also play in
mood disorders. Biological & genetic factors can be exacerbated based on the individual’s environment (epigenetics). It
also emphasizes that individuals with mood disorders are unwanted in society and thus the only treatment would be to get
rid of them. This of course is seen as unethical.

Depression Defined
1) List the DSM criteria for diagnosing major depression.
a. anhedonia (lack of interest)
b. appetite change (eat a lot or a little)
c. motor activity reduced (psychomotor retardation)
d. trouble concentrating
e. feeling of worthlessness & guilt
f. thoughts of self harm or suicide

2) Explain why Serotonin, Dopamine and Norepinephrine are strong neurotransmitter modulators of mood.
a. Serotoninà pleasure pathway; depression inhibits pleasure, only obsession w/ grief
b. dopamineà regulates motor areas; depression can produce anhedonia, limiting interest
c. norepinephrineà lack of it induces lethargy
3) Describe the process of electrochemical neural signaling.
a. The dendrites (receiving end) receive the chemical signals from other neurons. To send information from one
neuron to another, the neuron sends electrical signals along the axon to the terminal synapse. The myelin sheath, covers
the axon & leaves a few gaps within the axon known as the nodes of Ranvier. These nodes enable electric signals to
travel quickly to the synapse. The synapse is where the neurotransmitters (chemical signal) are released to be picked up
by the dendrite of the other cell.

4) Evaluate how your opinions on electroshock therapy changed after hearing Sherwin Nuland’s testimony.
a. Prior to this class, I knew that electroshock therapy was used as a last resort to depression when all other
treatments were ineffective. I perceived it to be a bit unethical because of how media portrayal of ECT would reflect on
the lack of consent that there was in ECT. After researching and hearing Dr. Nuland’s testimonial of ECT, I think ECT can
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The Neurobiology of Depression
1) Describe the discovery of antidepressants.
a. In the early 20th century, there was an epidemic of tuberculosis; sanitariums were organized to ensure those
infected were isolated. Patients were kept near open windows for fresh air
b. the first trial of TB treatment involved iproniazid & isoniazid. Two weeks after administrating the treatment,
patients still had TB in their lungs, but the patients were in a much happier mood
c. The patients were depressed during their time at the sanitariums. This ultimately led to the discovery that there
could be pharmaceuticals that could treat depression.

2) Diagram the synthesis, storage and release of neurotransmitters from neurons.

a. Neurotransmitters are synthesized naturally & with the help of our diet. For example: tyrosine can be obtained
through chicken, turkey, fish, peanuts, cheese, yogurt & bananas. Tryptophan can be obtained through pumpkin seeds,
chocolate, chickpeas, bananas
- with chemical process, tyrosine turns to dopamine & tryptophan turns into serotonin
b. The neurotransmitters are uptake by vesicles to be stored in
c. Release of neurotransmitters are done with an activated electric signal that travels through an axon; Ca2+ enters
the cell, allowing the vesicle to fuse with the presynaptic membrane, ultimately allowing the vesicles to open and release
the neurotransimitter into the synaptic cleft
d. the post synaptic receptor gets ready to receive & then neurotransmitter binds to the receptor sites; this triggers
a reaction in the dendrite of the other neuron!
e. Things cant go on forever! Removing the neurotransmitter signal from the synaptic cleft can occur in two ways:
- Reuptakeà neurotransmitter is recycled & taken back to the presynaptic terminal with the help of
transporters
- MAOà these are enzymes that clear up the neurotransmitter all together
3) Describe the role of 5-HT, DA, NE and substance P in depression.
- A decrease in serotonin, dopamine, norepinephrine, & substance P causes depression
a. 5-HT (serotonin)à causes obsession with grief; a decrease in serotonin allows the perservance loop to be
ongoing
b. Dopamineà decrease in dopamine leads to anhedonia (lack of interest)
c. Norepinephrineà decrease in NE leads to lethargy, psychomotor retardation, among other motor difficulties
d. substance Pà a decrease in substance P can lead to the person more sensitive to pain

4) Explain ways in which thyroid function can mimic depression.

a. 20% of depressions could be undiagnosed hypothyroidism
b. the symptoms associated with depression (trouble concentrating, fatigue, lethargy) are identical to someone
with hypothyroidism

5) Evaluate how steroid hormones (estrogen, cortisol) modify risks for depression.
a. Estrogenà estrogen increases around ovulation; on these days you usually feel good; a drop in estrogen
however, can make you feel groggy; this drop is usually associated with an increase in progesterone; a decrease in both
hormones leads to super feeling of grogginess
-low estrogen is associated with post partum depression & menopause
b. Cortisolà an increase in cortisol is associated with an increased risk of depression; cortisol is a stress hormone,
it is released when your amygdala senses a threat; fight or flight kicks in cortisol levels rise to prepare you to fight or flight;
afterwards, the excess cortisol makes you feel lousy and tired; an excess cortisol puts you at risk for depression
6) Describe the relationship between sleep and depression.
a. people who are continually depressed have difficulty in achieving stage 4 sleep
7) Make a hypothesis for the underlying causes of depression based on patient behavior.

Sociocultural Aspects of Depressive Disorders

1) Read a map showing global rates of depression.
a. Depression burden is illustrated the highest in Western nations, especially in the United States
b. depressive disorders have higher prevalence rates in women than men.
c. the age of onset for depression is usually 20-24 & weans at ages 75 & up.
2) Hypothesize how western and eastern cultural practices may influence depression rates.
a. Western cultural practices are rooted in Judeo-Christian values
- guilt & sinà feelings of guilt associated with the individual at fault which can exacerbate feelings of
worthlessness
-The philosophy of the West emphasizes that there is an ideal form of being you should aspire to be
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 -individualist cultures found in many Western nations promote individualism, encouraged to take
responsibility for their actions & promote individual goals that do not have to cater to no one else but you.
b. Eastern Cultural practices tend to see symptoms we associate with depression as not depressive at all; i.e.
Buddhism & norm to feel sad, it is part of the process of life
- Many Eastern cultures are collectivist. They encourage people to do what is best for the community and
promote rules stabilizing order
- the feeling of unity relieves the feeling of worthlessness; you have a purpose to make your community
happy
c. Hollywood norms of romanticizing depression as a trend was influenced by phenomenology
3) Give examples of cultural differences in presenting symptoms of depression.
a. Latin & Mediterranean culturesà nerve pain & headaches
b. East Asian culturesà abdominal pain, fatigue, feelings of inner pressure
c. Middle Eastern cultures & Hopi Indianà heart problems & “heartbroken”
4) Define “culture-bound syndromes”.
a. disorders that are identified & exist within a culture; symptoms may be widespread but depending on the cultural
norms & values, a syndrome may be identified as such if it violates the norms of that culture
b. ex. Brain Fag in West Africa; Studiation Madness in Trinidad
5) Define “phenomenology”.
a. the idea that says humans seek meaning in a world where there’s no meaning
6) Describe a gene that can influence depression risk.
a. the 5-HTT is known as the serotonin depression gene
b. the allele combination determines the amount of transporters available during reuptake of neurotransmitter
c. it is expressed by the genotype LS or SS
d. having the short 5 HTT allele can indicate a greater amygdala activity & more? transporters
e. it also puts you the predisposition of lacking inhibitory feedback associated with frontal cortex, cingulate, &
amygdala
7) Evaluate how culture and genetics work together, both predisposing and protecting subjects from depression.
a. the global rates of the short S gene are reciprocal to the global distribution of unipolar depression
b. but these countries also encourage a collectivist culture
- the perceived high threat encourages people to stay & work in cohesion to prevent their societal
disruption
-in actuality, this means that the s allele is a protective factor
c. Individuals who had the SS allele who had a reliable mentor were at no higher risk for depression
d. SS individuals who perceived good social support and had been exposed to a natural disaster did not have a
higher risk of developing depression

Pharmacology and Therapeutics of Antidepressants

1) Describe the mechanism of the following antidepressants: MAOIs, Tricyclics, SSRIs, SSNRIs, SNDRIs, 5-HT2
antagonists.
a. MAOIsà monoamine oxidase inhibitors; they inhibit the enzyme responsible for clearing neurotransmitters at
synapse directly interfering with reuptake & allowing an excess of neurotransmitters
b. Tricyclicsà responsible for blocking transporters associated with reuptaking the neurotransmitter back to the
presynaptic terminal
c. Selective Serotonin Reuptake Inhibitors (SSRIs) à blocks serotonin transporters; more serotonin at the synapse
d. Selective Serotonin Norepinephrine Reuptake Inhibitors (SSNRIs)à blocks serotonin & norephinephrine
transporters
e. Selective Norepinephrine Dopamine Reuptake Inhibitors (SNDRIs)à block norepinethrine & dopamine
transporters; more norepinephrine & dopamine
f. 5-HT2 antagonistsà
2) Compare and contrast the effectiveness of antidepressant drugs with placebo effect.
3) Evaluate the effectiveness of cognitive therapy in association with antidepressant treatment.
a. Mirror Neuron Hypothesis
- your conscious thought sits at the frontal cortex, it is what you know for sure
- subconscious is at limbic system, these are thoughts that you are unaware of happening until you begin
to be obsessed with them.
- the idea behind this theory is that your therapist who has a healthy conscious thought, listens to the
concerns caused by perservance loop & attempts to suppress this loop by strengthening your frontal cortex & be able to
overcome subconscious with conscious.
4) Describe ways in which new technology is changing depression treatment.
a. Vagus nerve stimulationà activating vagus nerve hits nearly all nerves of parasympathetic system (slow acting),
counteracting
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b. Transcranial magnetic stimulationà targeting specific regions of brain in stimulating activity
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 c. deep brain stimulationà implanting a cord that electrically stimulates the “deep areas” of the brain
d. Cingulotomyà surgical procedure that lesions your cingulate cortex, interfering with perservance loop
(obsession & emotion ass. With depression).
e. Electroshock therapy
5) Diagnose cheese effect and serotonin syndrome. Compare and contrast the causes.
a. Many aged foods such as aged cheese & aged meats have tyramine, a molecule that mimics the effects of
serotonin and thus the peripheral nervous system thinks there is norepinephrine, beginning the sympathetic response to
help you move! MAOs clear neurotransmitters from synapse while MAOIs inhibit the MAO from clearing it. This allows
an excess of neurotransmitter, in this case norepinephrine to be in the synapse. As a result, your sympathetic nervous
system is hyperactive, increasing heart rate & dilating pupils. Hence, taking MAOIs increase your chances of having
cheese effect as you have an excess of sympathetic activating neurotransmitters!
a. Serotonin syndrome is similar to cheese effect in such that taking MAOIs with other serotonergenics exacerbate
it, but in this case, it is an excess in serotonin. MAOIs inhibit serotonin transporters from working and already with the
effects of the serotonergenics, you have an excess in serotonin; dilated pupils, diarrhea, hallucinations, increase in
reflexes

Genetic & Environmental Contributions in Depression

1) Identify what percentage of depressive episodes are genetic.
a. About 30-40% of depressive episodes are genetic
b. 10-25% of women are affected while 5-12% of men are affected
2) Interpret twin studies results showing correlation of heritability and depression.
a. The study illustrates that because monozygotic twins share the same genes, if a twin develops depression,
the other identical twin is also likely to develop depression; the evidence of heritability and depression is
stronger in identical than fraternal twins
b. Women identical twins are much more likely to develop depression than their male counterparts
3) List 5 lifestyle factors and 5 social interaction factors that increase the risk of a depressive episode.
a. Lifestyle factors that increase depressive episode:
i. Overwork
ii. Poor sleep
iii. Drug abuse
iv. Lack of leisure time
v. Poor diet
b. Social Interaction Factors that increase depressive episode:
i. Serious trauma i.e. rape, neglect
ii. Death of a loved one
iii. Social failures i.e. broken friendships
iv. Chaotic, unsafe home life
v. Moving into another city
4) Evaluate ways in which early life stressors and exposure to trauma increase risk for depression. Describe 3
physiologic responses that may be altered.
a. When an individual is exposed to an early life stressor (i.e. abuse, loss of a parent, neglect), it can alter a
child’s brain development (critical period!)
b. This can alter a person’s predisposition to depression, altering the changes in brain development
c. Conseuqeneces of early life stressors include
i. Evelvated glucocorticoids
ii. Decreased hippocampus volume
iii. Elevated amygdala reactivity & sensitive amydgala
5) Compare and contrast how genes can increase or protect a subject from depression.
a. Carries of the short 5-HTT allele are predispositioned in experiencing a depressive eipisode; of course an
individual’s environment can alter the expression of the gene.
b. Having the short 5-HTT allele and experiencing early stressors can increase your risk of developing a
depressive episode
c. Having a polymorphism in the corticotrophin receptor 1 (CRHR1) gene illustrates the protective factor
against early life stress/abuse

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