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Study Guide Questions
Information from notes/power points
Information from textbook
Chap 8. Nerve cells and electrical signaling
1. Describe the components and overall functional organization of the nervous system (i.e., CNS & PNS).
The nervous system consists of the central nervous system and the peripheral nervous system,
● Central nervous system: the brain and spinal cord
● Peripheral nervous system: composed of the motor division and the sensory division.
○ Sensory division: afferent impulses, skin and organs respond to stimuli & refer that info back to the CNS which will trigger some kind of output.
○ Motor division: autonomic and somatic divisions
■ Autonomic division: involuntary motor output, innervates
smooth and cardiac muscle, consists of the sympathetic Don't forget about the age old question of In chemistry, what is the function of hybridization?
and the parasympathetic divisions
● Sympathetic division: fight or flight, increases HR &
LVR, decreases digestion, pupils dilated, excretory
activities inhibited, metabolic rate increases
● Parasympathetic divisions: rest and digest,
digestive tract is active, blood pressure & HR & LVR
is low, pupils constricted
2. Describe the general anatomy of a neuron in functional terms; that is, describe the function of the dendrites and cell body compared to the axon hillock and axon. How is the axon terminal functionally different from the rest of the neuron? We also discuss several other topics like How did kepler challenge the earth centered model?
Don't forget about the age old question of When are polygraph tests illegal to use?
● Dendrites and cell body: receive afferent (incoming) impulses ● Axon hillock: trigger zone, where an action potential is generated ● Axon: nerve fiber, efferent (outgoing) impulses, where an action
potential is conducted to the target cells at the end of the axon 3. What is the ionic basis for the resting membrane potential; how is it produced and maintained? What are the ways that it can be altered (i.e., hyper- vs depolarization)? If you want to learn more check out Why was the american revolution considered a process instead of an event?
● Resting membrane potential: difference in voltages across the membrane, maintained through active transport of Na+ out and K+ in maintains the gradient and the fixed anions inside makes intracellular concentration relatively negative.
● It can be altered by altering the membrane permeability, or the selective manipulation of ion channels (particularly Na/K)
● Depolarization: inside of the membrane becomes less negative ● Hyperpolarization: inside of the membrane becomes more
negative
○ This makes it more difficult to trigger an AP because you
will need a suprathreshold stimulus to reach threshold
4. Graded/local potentials:
● Properties
i. Short-lived, local changes in the membrane potential, If you want to learn more check out What is the inverse function of the exponential function?
depolarizations or hyperpolarizations
● Location
i. Dendrites and cell body
● Duration
i. They are short-lived, but can summate
● Direction of change of membrane potential
i. Travel short distance loosing strength as they travel, from the cell body or dendrites to the axon hillock or “trigger zone”;
waves of depolarization move through the cytoplasm until they reach the trigger zone
● Intensity over distance: local potentials “degrade”
i. Magnitude decreases with distance from the source, the farther away from the axon hillock, the more it will decrease over time
as it travels to the axon hillock
1. A stimulus at the dendrites or cell body will degrade more We also discuss several other topics like Where were oldowan artifacts excavated?
over time as opposed to a stimulus at or near the axon
hillock.
a. Axodendritic synapses: synapses at the dendrites
b. Axosomatic synapses: synapses at the cell body
c. Axoaxonic synapses: synapses at the axon hillock,
the most likely to generate an AP because it
doesn’t have to travel to the hillock
● Temporal vs spatial summation define these terms
i. Two or more axons can summate (combine)
1. Temporal summation: two stimuli from one axon terminal
combine to form a suprathreshold stimulus
2. Spatial summation: two stimuli from two different axon
terminals combine to form a suprathreshold stimulus
a. Spatial summation of EPSP and IPSP: an inhibitory
and an excitatory response summate to sort-of
counteract each other, most often results in a
subthreshold stimulus and therefore no AP
5. The Action Potential: compare and contrast with Graded Potentials i. High intensity (above threshold) local/graded potentials result in an action potential
ii. they are always depolarizations
iii. they are long-lasting, travel long distances and do not degrade over distance
iv. magnitude is fixed, all-or nothing
v. Occur only along axons
Local/graded potential
Action potential
local changes in
Result from
membrane potential
suprathreshold
local/graded potentials
Depolarizations or
hyperpolarizations
Always depolarizations
Length
Short-lived
Long-lasting
Distance
Travel short distances to the axon hillock, degrade as distance from the
source increases
Travel long distances, do not degrade over time
Magnitude
Can vary depending on the stimulus intensity
Fixed magnitude, all-or nothing
● Be able to graphically depict the change in potential across the membrane during an AP
● Label the axes of the graph with accurate absolute values for membrane potential &
Time
Resting, depolarization, repolarization, hyperpolarization, resting ● What are the ionic events that produce each phase of the AP? i. Early depolarization phase: local potentials reach threshold
ii. Depolarization phase: at threshold, voltage gated Na channels open, influx of Na depolarizes membrane
iii. Repolarization phase: “fast” Na gates close and “slow” voltage gated K gates open (at the peak). Efflux of K causes
repolarization
iv. Hyperpolarization phase: K gates close, but they are slow, so potential goes below resting membrane potential
v. Resting phase: membrane returns to resting membrane
potential.
● Define absolute and relative refractory periods
i. Absolute refractory period: no further depolarization can be
stimulated, no matter how strong the stimulus. AP can only
move away from the point of origin
ii. Relative refractory period: occurs during the phase of
hyperpolarization or “undershoot” where another AP can be
triggered but the stimulus needs to be a stronger suprathreshold stimulus
6. Propagation
● Role and properties of myelin & nodes of Ranvier
i. Myelination produces the fastest velocity of AP
ii. Nodes of ranvier: the Na channels are concentrated at the
nodes, the AP jumps from node to node: if the nodes are too far or too close, the AP will die
● What is saltatory conduction?
i. Jumping conduction, the AP jumps from node to node
Chap 7: Synaptic Integration
1. Describe the sequence of events beginning with the depolarization of the membrane at the axon terminal & ending with binding of neurotransmitters on the postsynaptic membrane.
a. Depolarization causes voltage-gated Ca channels to open
b. Ca moves into the presynaptic cell
c. Synaptic vesicles fuse with the membrane
d. Exocytosis of neurotransmitter (as they fuse with the membrane, the synaptic vesicles dump their product into the synaptic cleft
e. Neurotransmitter-receptor interaction: on postsynaptic cell, the neurotransmitter binds to receptors that have a tight association with ion channels
f. Opening of postsynaptic ion channels (ligand/chemically gated channels): different kinds of channels depending on where you look on a neuron
g. Degradation of neurotransmitter (it disappears)
2. Postsynaptic potentials: 2 types
a. Neurotransmitters open chemically-gated channels on the postsynaptic cell
b. This results in ion flow across the membrane and produces
local/graded potentials
c. Two kinds:
i. Excitatory postsynaptic potentials (EPSPs): depolarizations from the Na influx (opening of Na channels)
ii. Inhibitory postsynaptic potentials (IPSPs):hyperpolarizations from K influx (opening of K channels)
1. This is good because it “turns down” some neural
pathways → we don’t want them all firing at once
• EPSP: what is the ionic basis for an excitatory response? Opening of Na channels
• IPSP: opening of K channels
1. Receptor-mediated neurotransmitter responses at the synapse ● Role & response of nicotinic receptors to ACh
i. Always an EPSP, initiates skeletal muscle contraction
1. ACh binds to the receptor, Na/K channels open
2. Na floods into and K flood out of the cell = EPSP
3. Result: a local/graded depolarization of the membrane
4. Dissociation of neurotransmitter/receptor complex (un
attach themselves) → released AChE
5. AChE degrades ACh (breaks it down to its constituents)
6. Choline is reabsorbed by the presynaptic cell
7. Resynthesis of ACh in presynaptic axon terminal, ready for
release at next AP
8. Closing of the Na/K channel, ready to occur again
● Muscarinic receptors: G-protein mediated response to
neurotransmitters
i. Either an EPSP or an IPSP
1. G protein-coupled receptors linked to second messenger
systems , response varies with the receptor type
● Poisons and specific drug effects at the axon hillock or synapse (e.g., curare, “nerve
gases,” tetrodotoxin [TTX], etc.)
● Botulinus toxin: peptide that blocks release of ACh, used
cosmetically as Botox, the most toxic substance known to
science
● Curare: inhibits ACh receptor interaction, induces paralysis of skeletal muscle, blocks ACh binding at NMJ, will knock you out ● Krait snakes: (alpha-bungarotoxin) binds to nicotinic ACh
receptors, will knock you out
● Nerve gasses (SARIN): inhibit the breakdown of ACh (inhibits AChE), which leads to a accumulation of ACh in the synapse, induce spastic paralysis - hideous death (sarin gas)
● Tetrodotoxin (TTX): found in puffer fish liver or gonads (fugu), paralyzes its victims, inhibits voltage gatedNa channels in motor neurons systematically
2. Types of neurotransmitters: describe each
Neurotransmitters are chemical substances that are released at axon terminae that cause changes in membrane permeability in postsynaptic cell ● ACh:
i. acetylcholine, promotes EPSPs at the neuromuscular junction (skeletal muscle)
ii. Promotes EPSP or IPSP in autonomic NS (smooth and cardiac) iii. Binds to specific receptors on the postsynaptic membrane 1. Two types of receptors:
a. Nicotinic receptors (always EPSP)
b. Muscarinic receptors (either EPSP or IPSP)
● Biogenic monoamines (e.g., serotonin, tyrosine-derived
catecholamines [dopamine, NE,E])
i. Serotonin: neurotransmitter in CNS, derivative of tryptophan, implicated in mood, behavior (low levels = depression)
1. Prozac and other SSRIs: blocks serotonin reuptake by
presynaptic cell
ii. Tyrosine derived catecholamines:
1. Dopamine:
a. In CNS, associated with reward pathways
b. Degeneration of dopamine-producing neurons in
brain = parkinson’s disease
c. Many drugs trigger dopaminergic (reward)
pathways
d. Associated with addiction
2. Norepinephrine and epinephrine
a. CNS and PNS
b. Fight or flight arousal response
c. BP, HR, LVR all increase
d. Autonomic sympathetic response
● Others (various amino acids, NO, etc.)
i. Amino acids: several amino acids function as neurotransmitters in the CNS
1. Glutamate is the primary excitatory neurotransmitter in
the CNS
ii. Peptides: many are co-secreted with other neurotransmitters 1. Substance P involved in pain pathways, opioid peptides
(enkephalins, endorphins) involved in pain relief, etc.
iii. Purines: bind to G protein-coupled receptors
iv. Gasses: Nitric oxide (NO): diffuses freely into the membrane rather than binding to a receptor
v. Lipids: bind to g protein-coupled receptors
Chap 9: CNS
1. Terminology (nuclei vs ganglia, tracts vs nerves)
a. Nuclei vs. ganglia:
i. Nuclei: structures that contain a number of cell bodies in the central nervous system
ii. Ganglia: structures that contain a number of cell bodies in the peripheral nervous system
b. Tracts vs. nerves
i. Tract: collection of nerve fibers (axons) in the central nervous system
ii. Nerve: collection of nerve fibers (axons) in the peripheral
nervous system
2. Structure of a spinal nerve (dorsal and ventral roots, ganglia, etc.) a. 31 pairs attached to the spinal cord
b. Doral roots and ventral roots
i. Dorsal root: afferent with a ganglion (sensory impulses only) 1. Sensory neuron cell bodies in dorsal root ganglion
ii. Ventral root: efferent (no ganglion, motor impulses only)
iii. Ventral horn: somatomotor neuron cell bodies in ventral horn iv. Lateral horn: autonomic motor neuron cell bodies in lateral horn 3. Organization of gray and white matter in spinal cord
a. In spinal cord, white matter is superficial, it has myelinated fibers / tracts
b. Grey matter is deep, it has unmyelinated fibers and cell bodies, structured in a butterfly shape
1
BIOL 224 Review MT 2 Fall 2018
Chap 10: Sensory Systems
1. Signal transduction in sensory systems
a. Sensory receptors transduce (change) energetic stimuli from the environment into neural impulses that are interpreted by our CNS
2. Receptor physiology
a. Sensory neurons have receptive fields: they are activated by stimuli that fall within a specific physical area
i. One receptive field is associated with one sensory neuron which synapses with one CNS neuron
1. Multiple receptive fields can overlap or transmit to the
same secondary sensory neuron, which is what
sometimes causes two points to be interpreted as one
3. Classification and types of receptors
a. Classified by:
i. Location of receptor: source of stimulus
1. Exteroreceptors: stimuli from external environment
2. Viscero/ interoceptors: respond to stimuli from inside the
body
3. Proprioceptors: in musculoskeletal organs
ii. Type of stimulus: sensory receptors respond to specific
modalities
1. Mechanoreceptors: respond to mechanical stimuli
2. Photoreceptors: respond to light stimuli
3. Thermoreceptors: respond to changes in temperature
4. Chemoreceptors: respond to chemical stimuli (smell, O2,
pH) → smell and taste
5. Nociceptors: pain receptors
4. Lateral inhibition
a. Increases the contrast between activated receptive fields and their inactive neighbors, is another way of isolating the location of a stimulus
i. The secondary sensory neuron inhibits other secondary sensory neurons around it, creating a greater contrast between the one and its neighbors, which allows for a stronger perception
5. Sensory adaptation (tonic vs phasic responses)
a. Phasic receptors: adapt to constant stimuli, rate of firing slows over time (temp, smell, touch), no longer responsive to stimulus
i. Rapidly adapt to a constant stimulus and turn off, they fire once more when stimulus turns off
b. Tonic receptors: do not adapt over time, (ex. pain), long lasting sensory input, this is good because we want to be aware of pain to survive i. Slowly adapting receptors that respond for the duration of a stimulus
6. Sensory neural pathways (3-neuron chain)
a. Stimulus and receptors of the afferent neuron (first order neuron) are in the peripheral nervous system
b. Synapse with the second order neuron in the spinal cord or brain stem c. Second order neuron synapses with the third order neuron in the thalamus
d. Third order neuron synapses in specific lobes of the cerebral cortex e. Both second order and third order neurons are in the CNS
7. Receptive fields
a. Depending on the size of the receptive field for a stimulus, we can pinpoint how many points were stimulated
i. If there is a large receptive field with multiple primary neurons synapsing with the same secondary neuron, we will interpret two stimuli as one, one signal will be sent to the brain
ii. If there are small receptive fields with one primary neuron synapsing with individual secondary sensory neurons, we will interpret 2 signals (two points being stimulated) to the brain. 8. The special senses
● Olfaction and taste: CN mediation, basic taste modalities, receptor-mediated responses to chemical stimuli
○ Olfaction and gustation are complementary senses
○ Taste (gustation): tongue and taste buds, gustatory receptor cells with sensory “hairs” (microvillae) (Note: taste maps are not entirely correct) ■ Sensory innvervation by:
● CN 7 (facial)
● CN 9 (glosopharyngeal)
■ Basic taste modalities:
● Salty: Na+ triggers salt receptors, anion modulates
● Sour: H+ triggers receptors (all acids taste sour)
● Sweet: many organic molecules
● Bitter: alkaloids (often poisons), low threshold
● Umami: amino acids, nucleotides, MSG
● Water?
● Sweet, bitter and umami receptors are g-protein
interactions (second messenger systems, associated with
opening of voltage gated Ca++ channels and Ca++
influx)
○ Olfaction (smell): a 3 neuron pathway
■ Mediated by special sensory receptors in dorsal portion of nasal cavity
■ Olfactory receptors are mitotic (only neurons that actively regenerate)
■ Respond to dissolved chemical stimuli
■ CN 1 projects directly onto cerebrum
■ Many olfactory receptors are associated with g proteins
● Equilibrium & the vestibular apparatus of the inner ear: otolith organs w/hair cells, semicircular canals: hair cells in the cupula. Impulses to brain via vestibular branch of CN VIII.
○ Equilibrium: a gravitational orientation
■ Mediated by the vestibular apparatus
● Vestibular apparatus has 2 parts:
○ Sacculus & utriculus (saccule and utricule)
■ Consists of:
● Macula (“spot”) with hair cells
○ Hairs embedded in gel-like
otolith membrane
● Otoliths (“ear stones”) of CaCO3
○ Detect linear acceleration/
internal motion. Ex: position of
the head or movement of the
head
○ Semicircular canals:
■ 3 semicircular canals in 3 different planes
■ Fluid-filled (endolymph)
■ Swelling at the base of the canals = ampulla
■ Sensory hairs located in the crista ampullaris
■ Hairs embedded in gel-like cupula
■ Sensitivity to circular motion (rotation)
■ Part of the inner ear
■ Neural input from CN 8
■ Sensory receptors are within a fluid-filled labyrinth
■ Specialized hair cells receive sensory info
● Ears and hearing: mediated by transmission of sound from outer ear to tympanic membrane. 3 middle ear bones (name them). Oval window transmits vibrations to fluid- filled (endolymph) cochlea. Hair cells embedded in basilar membrane, “hairs” embedded in tectorial membrane. Vibration in fluid bends hairs, trigger neural impulse.
○ Sound waves are funneled by the auricle & external auditory canal ○ They are transferred to the tympanic membrane (eardrum) ○ Then are carried through the air-filled middle ear by 3 tiny bones (ossicles)
■ Malleus (‘’hammer’’)
■ Incus (‘’anvil’’)
■ Stapes (‘’stirrup’’)
○ Vibrations enter the inner ear at the oval window
○ Carried into the fluid-filled (endolymph) cochlea (seashell) ○ Sound energy enters the cochlea
○ Hair cells are embedded in the basilar membrane and their “hairs” are embedded in the tectorial membrane
○ Vibrations in endolymph cause the hairs to bend which triggers an action potential
● Eyes and vision: define/understand the following
○ Accommodation (presbyopia), myopia, hyperopia, emmetropia ■ Accommodation: ability to keep an object in focus as its relative distance changes
● Facilitated by changing shape of lens and altering the
pupil size
● Presbyopia = inability to accomodate
■ Emmetropia: normal (20/20) vision, image focuses sharply on retina
■ Myopia: nearsightedness (inability to see far)
● Eyeball too long (out of round or stretched)
● Image focuses in front of the retina
■ Hyperopia: farsightedness (inability to see near)
● Eyeball too short/foreshortened
● Image focuses behind the retina
○ Pathway of light from cornea...to retina: list the structures/regions of the eye it passes through on the way to photoreceptors. ■ Light passses thorough the cornea and pupil and is focused on the retina by the lens. The retina is what contains the
photoreceptors. Light must pass through ganglion cells, amacrine cells, bipolar and horizontal cells to reach the photoreceptors in the deepest layer of the retina.
● Cornea → pupil → lens → retina (ganglion cells → amacrine cells → bipolar and horizontal cells → photoreceptor cells) ■ Cornea: outer fibrous tunic layer
■ Choroid: middle layer, vascular tunic (blood supply)
■ Retina: inner layer, neural tunic
■ Iris: pigmented part of the eye, circular and radial muscle that controls the amount of light entering through the pupil
■ Pupil: hole in the iris where light enters
■ Lens: clear, acellular, crystalline protein that focuses light on the retina
■ Optic disc: blind spot where the cranial nerve (CN 2) exits the eye
○ Role of rods and cones: how are visual stimuli transduced by photoreceptors? How is this pattern different from most receptor mediated responses?
■ Rods: receive dim light/ peripheral vision
● Most numerous in the periphery
● Contains the visual pigment rhodopsin
● Light causes the dissociation of rhodopsin which changes the permeability of the cell membrane (hyperpolarization) and triggers an AP in the ganglion cell
■ Cones: receive bright light/ high resolution color vision ● Most dense in the macula lutea/ fovea (center) (site of visual focus)
● Contain photopsins
● Three types of cones (photopsins) absorb different
wavelengths (blue, red, green)
■ Approximately half of visual information crosses over to the other side of the brain
● Visual stimuli from the left field of view strikes the right side of the retina, which means all visual data from the
left field of view is processed in the right visual cortex ● Visual stimuli from the right field of view strikes the left side of the retina, which means all visual data from the
right field of view is processed in the left visual cortex
○ Dissociation of rhodopsin in rods (opsin, retinene)
■ Rods contain the visual pigment rhodopsin (a compound molecule made of opsin and retinene)
■ Light causes the dissociation (breaking apart) of rhodopsin into opsin and retinene
■ This changes the permeability of the cell membrane (a
hyperpolarization) which triggers an AP in the ganglion cell
○ Cones: photopsins (RGB), photoreceptors in fovea centralis.
■ Cones contain photopsins
● There are 3 kinds of cones or photopsins that absorb
different wavelengths of light
○ Red, green and blue
■ Cones receive bright colored light and are most dense in the macula lutea or fovea centralis which is the sight of visual focus ○ What is the “blind spot”? What physical conditions result in glaucoma? ■ Optic disk = blind spot, it is where the CN 2 exits the eye, there are no photoreceptors here which is why we call it the blind spot ■ Glaucoma: chronically high intraocular pressure
● Caused by an increase in pressure in the anterior
chamber
● Slow drainage of aqueous humor
● Results in damage to ganglion cells that form the optic
nerve
● Visual field loss, untreated can lead to blindness
Chap 11: The ANS the involuntary nervous system , innervates smooth and cardiac muscle
● Describe the anatomy of an autonomic motor unit (2 neuron chain, but PS, S exit from different locations—see below)
○ An autonomic motor unit is a 2 neuron chain with a ganglia (ganglia= a group of cell bodies in the PNS, where first order and second order neuron synapse
■ Preganglionic (1st order) neuron cell body in the brain or spinal cord
■ Postganglionic (2nd order) neuron in autonomic ganglion
● Postganglionic axon goes to the effector organ
● Sympathetic vs parasympathetic divisions of the ANS
○ Physiological responses (“fight or flight” vs “rest and digest”) ■ Parasympathetic:
● Couch potato (rest and digest)
● Digestive tract is active
● BP, HR, LVR all low
● Pupils constricted for near vision
■ Sympathetic
● Fight or flight
● Increased HR and LVR
● Decreased digestion
● Pupils dilated
● Increased metabolic rate
● Excretory activities inhibited
○ Location fibers exit CNS in each?
■ Parasympathetic: craniosacral → fibers emerge from brainstem and sacral spinal cord
■ Sympathetic: thoracolumbar→ fibers emerge from thoracic lumbar spinal cord
○ Relative length of pre- and postganglionic fibers?
■ Parasympathetic: 1st order neuron is long and 2nd is short ■ Sympathetic: 1st order is short and 2nd order is long ○ Neurotransmitters of the ANS: ACh, NE
■ All preganglionic fibers release ACh → always elicits an EPSP ■ Parasympathetic: postganglionic fibers release ACh → effect depends on receptor
■ Sympathetic: secretes NE → usually EPSP
○ Receptors: nicotinic ACh receptors where? Muscarinic ACh receptors where?
■ Nicotinic ACh receptors: on all postganglionic neurons, effects always excitatory
■ Muscarinic ACh receptors: on all parasympathetic target organs ■ Adrenergic receptors: on sympathetic target organs
○ Adrenergic receptors: a1, a2, b1, b2 (NE binding receptors) ■ Alpha: usually stimulatory effects
● A1: vasoconstriction, dilate the iris, relax the gut
● A2: often on presynaptic membrane, may inhibit
■ Beta: often inhibitory effects
● B1: increase rate and force of heartbeat
● B2: broncho- and vasodilation
○ Receptor-mediated responses at the target tissues: excitation vs inhibition
■ Nicotinic receptors: always excitatory
■ Muscarinic receptors: excitatory or inhibitory
■ Adrenergic receptors:
● Alpha: usually stimulatory
● Beta: usually inhibitory
○ How does an autonomic neural pathway differ from a somato motor pathway?
■
Comparison of Autonomic and Somatic motor divisions
Autonomic
Somatic motor
Number of
neurons in
efferent path
2
1
neurotransmitter / receptor at
neuron-target synapse
ACh/muscarinic or NE/adrenergic
ACh/nicotinic
Target tissue
Smooth and
cardiac muscle,
glands, adipose
tissue
Skeletal muscle
Neurotransmitter released from
Axon terminals and varicosities
axon terminals
Effects on target tissue
Excitatory or
inhibitory
Excitatory only
Peripheral
components
found outside
the CNS
Preganglionic
axons, ganglia,
postganglionic
neurons
Axons only
Summary of
function
Visceral function, control of
metabolism
Posture and
movement
Differences between the parasympathetic and sympathetic divisions of the ANS
Parasympathetic
Sympathetic
Physiological
responses
Rest & digest (couch potato)
-digestive tract active -BP, HR, LVR all low -pupils constricted
Fight or Flight (fright or frolick)
-increased HR and LVR
-digestion process low
-Pupils dilated
-excretory activities inhibited
-metabolic rate
increase
Location fibers exit the CNS
Craniosacral
thoracolumbar
Relative length of pre and
postganglionic
fibers
1st is long and 2nd is short
1st is short and 2nd is long
NT release by
preganglionic
axons
ACh
ACh
NT release by
postganglionic
ACh
NE
axons
Receptor type on postganglionic cell body
Nicotinic
Nicotinic
Receptor type on effector
Muscarinic
Adrenergic
○
● Receptor mediated responses—how does NE trigger a cellular response at target tissues?
○ NE:
■ Action potential results in a depolarization that opens voltage gated Ca channels
■ Ca enters cell and triggers exocytosis of synaptic vesicles (NE is released to the synapse)
■ NE binds to adrenergic receptors on the target tissue and initiates a response
● How do certain drugs (e.g., albuterol) elicit a targeted receptor-specific response in the ANS?
○ Curare: blocks nicotinic receptors, muscle relaxant
○ Propranolol: beta-blocker, lowers heart rate,
■ Non-specific beta blockers, so it binds to B1 and B2
○ Albuterol: a B2 agonist, used to treat asthma (a bronchodilator) ○ Atropine: (belladonna) : inhibits muscarinic receptors, dilates pupils, inhibits contractions of gut muscles
○ How can non-specific B blockers like propranolol be potentially harmful in specific cases?
■ If someone with asthma and a bad heart is given a non-specific beta blocker it can actually cause an asthma attack