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SONOMA STATE UNIVERSITY / Biology / BIOL 224 / What is the ionic basis for the resting membrane potential?

What is the ionic basis for the resting membrane potential?

What is the ionic basis for the resting membrane potential?


School: Sonoma State University
Department: Biology
Course: Human Physiology
Professor: Nicholas geist
Term: Fall 2018
Tags: The, nervous, system, study, and guide
Cost: 50
Name: Midterm 2 Study Guide
Description: This exam covers the nervous system. Originally the skeletal muscle system was going to be on this exam, but Dr.Geist has taken it off.
Uploaded: 10/12/2018
14 Pages 26 Views 4 Unlocks

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Study Guide Questions  

What is the ionic basis for the resting membrane potential?

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  

What is saltatory conduction?

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  

How does an autonomic neural pathway differ from a somato motor pathway?

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  


○ 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  


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


local/graded potentials

Depolarizations or  


Always depolarizations





Travel short distances to  the axon hillock, degrade  as distance from the  

source increases

Travel long distances, do  not degrade over time


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 &


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  


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  


● 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  


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  


● 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)  


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  


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  


3. Proprioceptors: in musculoskeletal organs  

ii. Type of stimulus: sensory receptors respond to specific  


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++  


○ 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  


○ 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  


● Slow drainage of aqueous humor  

● Results in damage to ganglion cells that form the optic  


● 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


Somatic motor

Number of  

neurons in  

efferent path



neurotransmitter / receptor at  

neuron-target  synapse

ACh/muscarinic or  NE/adrenergic


Target tissue

Smooth and  

cardiac muscle,  

glands, adipose  


Skeletal muscle

Neurotransmitter released from

Axon terminals and varicosities

axon terminals

Effects on target  tissue

Excitatory or  


Excitatory only



found outside  

the CNS


axons, ganglia,  



Axons only

Summary of  


Visceral function,  control of  


Posture and  


Differences between the parasympathetic and sympathetic divisions of the ANS





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  


Location fibers exit the CNS



Relative length of  pre and  



1st is long and 2nd is  short

1st is short and 2nd  is long

NT release by  





NT release by  





Receptor type on  postganglionic cell  body



Receptor type on  effector



● 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

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