Chapter 10

The ANS innervates smooth muscle, cardiac muscle and glands and the tissues are often
referred to as visceral effectors because they are associated with the viscera (internal organs)
of the body

-autonomic motor neurons regulate visceral activities via excitation and inhibition, and can
function even if their nerve supply is damaged or cut

ANS consists of two main branches: the parasympathetic nervous system (PNS) and the
sympathetic nervous system, most organs receive nerves from both systems, this is known as
dual innervation, one system excites the organ while another inhibits it (e.g. PNS inhibits heart
rate, sympathetic excites heart rate)

PNS: rest and digest

sympathetic: fight or flight

ANS also made up of third branch, enteric nervous system (ENS)

An autonomic motor pathway is made up of two autonomic motor neurons and one visceral
effector (e.g. smooth muscle, cardiac muscle or a gland)
-the first neuron called the preganglionic neuron has its cell body in the brain or spinal cord, its
axon exits the CNS via a cranial or spinal nerve and then extends to an autonomic ganglion
where it synapses with the second neuron, the postganglionic neuron, which lies entirely in the
PNS and its cell body is located in the autonomic ganglion, its axon extends from the ganglion to
the visceral effector

-preganglionic neurons convey APs from the CNS to the autonomic ganglia
-postganglionic neurons convey APs from the autonomic ganglia to the visceral effector

-in PS preganglionic cell bodies are located in the brainstem and sacral regions of the spinal
cord, hence the PS is aka the cranial sacral division of the ANS
-PNS preganglionic axons exit the CNS via cranial nerves 3,7,9 and 10 and sacral spinal nerves
(S2-S4)
-terminal ganglia: where PS postganglionic axons extend to and are located close to or in the
walls of the visceral effector
-PS preganglionic axons are long and PS postganglionic axons are short

-in S preganglionic cells bodies are located in the thoracic and upper lumbar regions of the
spinal cord, aka thoracolumbar division of the ANS
-most S preganglionic axons extend to S postg neurons in the sympathetic trunk, while some
extend to S postg neurons in the collateral ganglia, from either the extend to the visceral
effector
-S preganglionic axons are short and S postganglionic axons are long
-some S pregang axons extend to chromaffin cellsin the adrenal medulla which release a
hormone mixture of about 80% epinephrine, 20% norepinephrine and trace amounts of
dopamine and these hormones intensify responses elicited by the SNS
-chromaffin cells are modified S postgang neurons that lack dendrites and axons, instead of
extending to another organ they release hormones into the bloodstream

SNS: T1-T12, L1-L2

neuroeffector junction (NEJ): the synapse between an autonomic postgang neuron and a
visceral effector

The organization of the NEJ differs from a typical neuron-to-neuron

synapse in two major ways:
1. The axon terminals of the postganglionic neuron lack synaptic end bulbs; instead, they
exhibit swollen regions called varicosities, which contain synaptic vesicles with
neurotransmitter.
2. In the effector, the receptors for the neurotransmitters are not confined to a specific
receptor region; rather, they are located along the entire surface of the cell.

Autonomic postganglionic neurons release neurotransmitters from varicosities, which are

swollen regions found at the ends of axon terminals.

When an action potential occurs in the autonomic postganglionic neuron, varicosities along the
length of the axon release neurotransmitters, which in turn diff use to receptors throughout the
effector. As a result, the autonomic postganglionic neuron affects a large area of the effector
tissue.

Release of neurotransmitters at the NEJ occurs:

1) an AP arrives at a varicosity of the autonomic postgang axon
2) depolarization causes calcium channels to open in varicosity membrane and calcium
flows inward
3) increased calcium triggers exocytosis synaptic vesicles and neurotransmitters are
released into the synapse
4) neurotransmitters diffuse across synapse and bind to their receptors in the effector
cell’s plasma membrane
5) the binding of the neurotransmitter to its receptor activates a G-protein, ultimately
leading to a response that either excites or inhibits the effector cell, depending on the
type of receptor and G protein pathway activated.

-neurotransmitters are removed from the NEJ via diffusion away from the synapse, degradation
by enzymes in the ECF or uptake into a nearby cell via active transport
Cholinergic neurons release acetylcholine (ACh) and include all PS and S preganglionic neurons,
most PS postganglionic neurons and S postganglionic neurons that innervate most sweat glands

-ACh binds with cholinergic receptors, integral membrane proteins in the postsynaptic plasma
membrane
-there are two types of cholinergic receptors, nicotinic ACh receptors and muscarinic ACh
receptors

Nicotinic ACh receptors are present in the plasma membranes of dendrites and cell bodies of
both PS and S postgang neurons, in the plasma membranes of chromaffin cells of the adrenal
medulla and in skeletal muscle at the NMJ, nicotine can bind to them, hence their name

Muscarinic ACh receptors are present in the plasma membrane of effectors (smooth muscle,
cardiac muscle and glands) innervated by PS postgang axons, and in sweat cells, muscarine
(mushroom poison) can bind to them

(Figure 10.6, p.g. 347)

Cholinergic effects are brief because ACh is quickly broken down via acetylcholinesterase
(AChE)

Adrenergic neurons release norepinephrine (NE) also known as noradrenaline. Most S

postganglionic neurons are adrenergic, adrenergic receptors respond to the binding of either
NE or E
-two types of adrenergic receptors, alpha and beta
-further subtypes of these receptors include alpha 1, alpha 2, beta 1, beta 2, beta 3

alpha 1&2: higher affinity for NE

beta 1: equal affinity for NE and E
beta 2: higher affinity for E
beta 3: higher affinity for NE

adrenergic effects are longer than cholinergic, and the activity of NE is terminated by MAO

Some autonomic neurons don’t release ACh or NEand are called nonadrenergic, noncholingeric
neurons, they can release neurotransmitters like adenosine, ATP, NO, somatostatin, substance
P and vasoactive intestinal polypeptide (VIP)

Autonomic tone (the balance between the PSNS and the SNS) is regulated by the hypothalamus

Structures that receive only S innervation: sweat glands, arrector pili muscles attached to hair
follicles in the skin, the kidneys, the spleen, most blood vessels and the adrenal medullae of the
adrenal glands
SLUDD – five PS responses, salivation, lacrimation, urination, digestion and defecation
PS responses reduce body functions that support physical activity
PS three decreases: decreased heart rate, decreased bronchial tube diameter
(bronchoconstriction) and decreased diameter of the pupils (pupillary constriction)

during SNS response, vigorous physical activity can be supported and rapid production of ATP
E situations can trigger SNS: exercise, excitement, embarrassment and emergency
some SNS responses include
 pupil dilation (increased diameter)
 heart rate, force of cotnraction and blood pressure increases
 bronchodilation to support faster breathing
 reduced urinary and digestive activity due to vasoconstriction of kidney and GI blood
vessels
 liver cells break down glycogen into glucose and fat cells break down triglycerides to
fatty acids and glycerol so body has proper molecules needed for ATP production
 blood glucose levels increase

Autonomic reflexes help maintain homeostasis and include a sensory receptor, sensory neuron,
integrating center, motor neurons and the effector
-integrating center for most autonomic reflexes located in the hypothalamus and brainstem
-cranial reflex: integration occurs in the gray matter of the brain
-spinal reflex: integration occurs in the gray matter of the spinal cord
-in autonomic reflex arc two autonomic motor neurons connect the CNS to an effector which is
either a smooth or cardiac muscle or a gland

-the hypothalamus is the major control and integration center of the CNS
The somatic nervous system regulates the activity of skeletal muscle and normally operates
under voluntary (conscious) control

-a somatic motor pathway is made up of a somatic motor neuron and skeletal muscle
-axons of somatic neurons that extend through cranial nerves innervate skeletal muscles of the
face and head
-axons of somatic neurons that extend through spinal nerves innervate skeletal muscles of the
limbs and trunk

-the NMJ is where the somatic motor neuron and skeletal muscle fiber synapse, ACh is released
here and has an excitatory effect which causes the skeletal muscle to contract
-motor end plate: the region of the muscle fiber plasma membrane opposite to the synaptic
end bulb and within it there are 30-40 million (nicotinic) ACh receptors
-synaptic end plate and motor end plate separated by synaptic cleft

-nerve AP arrives at synaptic end bulb of a somatic motor neuron

-calcium channels open and calcium enters synaptic end bulb which triggers release of ACh into
synaptic cleft
-ACH diffuses across synaptic cleft and binds to nicotinic receptors on motor end plate, binding
of two ACh causes sodium inflow into the cell
-sodium inflow causes motor end plate to depolarize and this is called an end plate potential
(EPP)
-EPP causes depolarization to threshold in the area and sodium channels open, influx of sodium
into muscle fiber causes muscle AP that leads to the contraction of the muscle fibre
-ACh then broken down by AChE which is located on the end plate membrane

NMJ events can be altered by chemicals such as botulinum toxin, alpha-latrotoxin, curare and
organophosphates
-botulinum toxic prevents ACh from being released in synaptic cleft and thus muscle
contraction does not occur and thus paralysis that can be deadly
-alpha-latrotoxin is found in black widow venom and causes the excessive release of ACh which
leads to overstimulation of skeletal muscles
-curare binds to nicotinic receptors on the motor end plate, preventing ACh from binding and
causing paralysis
Chapter 11

three types of muscle: skeletal, cardiac and smooth

skeletal muscle is striated and involved in voluntary movement, it is attached to bones and
moves parts of the skeleton
involuntary muscle control includes diaphragm moving for breathing, and muscles used to
maintain posture

only the heart contains cardiac muscle which is also striated and under involuntary control
autorhythmicity: built in rhythm of the heart

smooth muscle are nonstriated and under involuntary control

Functions of muscle:

-body movement
-stabilizing body positions (posture)
-storing and moving substances within the body – via sphincters and smooth muscle or cardiac
contractions
-generating heat via thermogenesis when muscles contract, shivering is the involuntary
contractions of skeletal muscles

Four special properties of muscles

1) electrical excitability – ability of both muscle neurons and cells to respond to stimuli and
generate APs
2) contractility – ability to forcefully contract when adequately stimulated
3) extensibility – ability to stretch without damage
4) elasticity – ability to return to its original shape and form before stretching

Muscle cells are called muscle fibers and each one is surrounded by a sheath of connective
tissue
Fascicles are little bundles of about 10-100 muscle fibers, also surrounded by connective tissue
Tendons are cords of connective tissue that attach the muscle to the bone

-a mature skeletal muscle fibre is about 10cm long and 10-100 micrometers in diameter, it also
has multiple nuclei due to the fusion of myoblasts during embryonic development, once this
fusion occurs, cells cannot divide so the number of skeletal muscles is set before birth and most
will last for the lifetime
-a few myoblasts exist and are called satellite cells and can help with regeneration of cells in
damaged muscle fibres but there isn’t enough for significant damage

sarcolemma: plasma membrane of a muscle fibre

myoglobin stores oxygen until its needed for ATP production and is only found in muscle
sarcoplasm: cytoplasm of muscle cell and contains glycogen, which can be broken down into
glucose to produce ATP

myofibrils: contractile elements of the skeletal muscle fiber, and within them there are thick
and thin filaments, both are involved in contractile processes
thin: 8 nm diameter, 1-2 micrometers long
thick: 16 nm in diameter, 1-2 micrometers long

-release of calcium from the terminal cisternae triggers muscle contraction

sarcomere: repeating units of a myofibril, Z discs separate one sarcomere from the next
A band extends the entire length of the thick filament, it is anisotropic and refracts polarized
light unevenly
M line: middle of the sarcomere
I band – contains thin filaments and no thick filaments, it is isotropic and refracts polarized light
evenly
zone of overlap: where thin and thick overlap, each thick filament surrounded by 6 thin, each
thin filament surrounded by 3 thick
H zone contains thick but no thin

Three types of muscle proteins: contractile, regulatory (switch the contraction process on and
off) and structural (keep thick and thin proteins in the proper alignment)

Two main components of contractile proteins: myosin and actin, myosin is in thick filaments
and actin in thin

myosin: two heavy chains and 4 light chains, two heads and a tail that is comprised of the two
heavy chains wrapped in a helix, each myosin head contains the light chains and an actin
binding site and an ATP binding site

thick filament: about 300 myosin molecules

individual actin cells – G actin, linked together in a chain = F actin

Two F-actin strands form a helix in a single thin filament and they are also covered in
tropomyosin and troponin
-each tropomyosin extends over 7 G-actin molecules
-in relaxed muscle, myosin cannot bind to actin as myosin binding site is blocked on actin by
tropomyosin, and tropomyosin is held in place on actin by troponin, a protein with 3 subunits,
one that binds to tropomyosin, one that binds to actin and one that binds to calcium, when
calcium binds to troponin, it causes it to change shape, which then results in a muscle
contraction as tropomyosin is moved away from myosin binding site on actin and myosin can
then bind to actin
Structural proteins: titin is the third most plentiful protein in skeletal muscle, after actin and
myosin, each titin molecule spans half a sarcomere, from a Z disc to an M line, it connects the Z
disc to the M line, helping to stabilize the position of the thick filament, this molecule also
accounts for extensibility and elasticity of the myofibril