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Identify the main differences between neurons and glia

Neurons cannot divide but can regenerate, where glia can do both. Neurons play a role in signaling with long cell processes, and glia play a supportive and signaling role with short cell processes. Both have secretory functions and membrane potentials, both are excitable except NEURONS = ACTION POTENTIALS, GLIA = TRANSMITTERS AND CALCIUM SIGNALING

Multipolar neurons

dendrites and one long axon - found in CNS - motor nerve in spinal cord ventral horn

Bipolar neurons

elongated cell body and two processes, one is the axon and the other ends with dendrites. Sensory neurons and retinal bipolar cells

Pseudo-unipolar neurons

two axon branches out of cell body, one is towards CNS, other to PNS. Sensory neurons in DRG and barroreceptor-sensitive cells in the nodose ganglion

Unipolar neurons

rare, axon arises from same spot with dendrites

Afferent Neuron


Efferent neuron



Neuron mediates information between afferent and efferent, CNS -> CNS or PNS -> PNS

Explain how the cytoskeleton traffics materials with neurons

uses cytoskeletal filaments: microtubules, neurofilaments/intermediate filaments and microfilaments

Fast anterograde transport

anterograde uses kinesin to take vesicles and mitochondria from soma to nerve ending

Slow anterograde transport

anterograde uses kinesin to take cytoskeleton molecules (really slow) and soluble proteins/enzymes from soma to nerve ending

Fast retrograde transport

anterograde uses dynein to take lysosomes, enzymes, recycled vesicular membrane from nerve ending to soma


found in the CNS - maintain cerebral flow and ionic and osmotic balances in the brain (form glial scars in Alzheimer's), store glycogen and supply neurons with lactate, regulate K+ in the microenvironment (spatial buffering or potassium siphoning), take up neurotransmitters from extracellular fluid, protect neurons from oxidative damage (SOD, CuZn, Mn-), maintaining homeostasis at the synapse, regulating neuronal signaling, release cholesterol (increases number of synapses and synaptic activity of neurons)


immunocompetent and phagocytic cells in the CNS, prevent injury, inflammation and disease, can release cytotoxic molecules and cause Alzheimer's, Parkinson's and MS


myelinate axons in the CNS

Ependymal cells

in the CNS - forms walls of ventricles, produce neurons and glial cells after stroke, can also contribute to glial scar formation after injury

Choroidal plexus epithelial cells

secretes CSF and transfers molecules from blood to CSF


bipolar cells that link CSF to neuroendocrine events

Perivascular astrocytes

associated with the neurovascular unit and are responsible for maintaining cerebral blood flow and ionic and osmotic balances in the brain

Schwann cells

myelinate axons in the PNS, have phagocytic activity and clear cellular debris. Immature S-cells are generated from S-cell precursors that originate from neural crest

Enteric glial cells

found in intrinsic ganglia of the digestive system, intimately associated with the neurons in the enteric nervous system, like CNS astrocytes - express neurotransmitter receptors and are most likely involved in neuronal communication

Satellite glial cells

Surrounds neurons in sensory, sympathetic and parasympathetic ganglia to regulate the external chemical environment

Tumors of glial origin

50% of all brain tumors, 25% of spinal cord tumors; CNS - astrocytoma, glioblastoma, oligodendroglioma, ependymoma; PNS - found on cranial nerves, spinal nerve roots, peripheral nerves and sympathetic chain ganglia - cells of origin are virtually always schwannoma (neuronal tumors are extremely rare in both the CNS and PNS)

GFAP (glial fibrillary acidic protein)

gene encodes intermediate filament proteins of mature astrocytes, Alexander disease is a mutation where high levels of GFAP is found in CSF, loss of myelin and degeneration of white matter in brain


hyperplasia and hypertrophy of reactive astrocytes in response to neuronal injury in the CNS - produces glial scars (limits axonal regeneration)

Pathological pain from astrocytes

secrete diffusible materials (interleukins, ATP, NO) can sensitize second order neurons in the spinal cord

Amyotrophic lateral sclerosis (ALS)

adult onset neurodegenerative disease that is characterized by the loss of brain and spinal cord motors - caused by mutations in SOD


loss of myelin sheath - MS, acute disseminated encephalomyelitis, Transverse myelitis, Alexander disease, chronic inflammatory demyelinating polyneuropathy, Guillain-Barre syndrome and central ponitine myelinosis, (pernicious anemia/B12 deficiency can lead to spinal cord degeneration)

Progressive demyelinating neuroinflammatory disease, HTLF-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP)

viral intrusion into the CNS and leads to death of myelin producing oligodendrocytes and degeneration of neuronal axons

Multiple Sclerosis (MS)

chronic inflammatory (autoimmune) demyelinating disease of the CNS (oligodendrocytes)

Guillain-Barre Syndrome

inflammatory demyelinating disease (polyneuropathy) of the PNS (Schwann cells) - Wallerian degeneration

Charcot-Marie-Tooth disorder (CMT)

mutations in gene for protein periaxin - leads to short myelin segments and reduced nerve conduction velocities

What viruses can use retrograde transport along microtubules to infect neurons

Herpes, polio, rabies, Parvo and HIV

Distinguish between the Erlanger and Gasser classification of fibers in a spinal nerve and that of Lloyd for muscle afferent fibers

(increase in diameter = increase in conduction velocity) E & G classification: A alpha, A beta, A gamma, A delta, B, C (from largest to smallest diameter of spinal nerve fibers), Lloyd: I-a, I-b, II, III, IV (from largest to smallest diameter of muscle afferent fibers)

What is the resting membrane potential of a neuron

-65 mV

What is the resting membrane potential of a skeletal muscle fiber

-90 mV

What is the resting membrane potential of a photoreceptor (rod)

-40 mV

Explain how the cell membrane components influence the separation of electric charge across the membrane and also the movement of charge across the membrane by ion flux

ions do not readily pass through the phospholipid bilayer and this endows the membrane to act as an electrical capacitator storing a charge difference across the membrane, charge moves by electrochemical and concentration gradients

Distinguish between the different means of ion flux across the membrane

passive (simple diffusion, channel mediated diffusion and carrier mediated diffusion) and active (active transport)

What happens if you raise extracellular [K+]

causes a reduction in the rate of potassium ion loss from the cell and interior becomes less negative (DEPOLARIZATION), also activates astrocytes, depolarizes astrocytes, and causes potassium siphoning of astrocytes

What happens if you lower extracellular [K+]

causes an increase in the rate of potassium ion loss from the cell and interior becomes more negative (HYPERPOLARIZATION)

Understand the importance of the differences between the intracellular and extracellular concentrations of sodium, chloride and potassium ions for muscle fibers and neurons

greater concentration difference for all ions in muscle cells compared to neurons

Describe the mechanisms that maintain these ionic distributions across the cell membrane

Na/K ATPase and other active transports

Explain how ion channels function as conductors in the cell membrane

potassium flux through open channels strongly influences the resting potential in neurons, chloride also participates in muscle cells, if sodium channels open and increase flux of sodium.

Review the Nernst equation in relation to the concept of ion equilibrium potential

Ex = (61.5/z) log {[X]o/[X]i} mV, Ex for an ion X is the particular value of membrane potential that counterbalances the ion's concentration gradient across the membrane

Review the concept of the electrochemical gradient for ionic diffusion across the cell membrane and apply this concept to new conditions

Electrochemical gradient = Vm - Ex (tells you which way the ions will flow)

List the typical values of the equilibrium potentials for sodium, chloride, calcium and potassium ions in skeletal muscle fibers and neurons

in neurons: Na=+62, K=-80, Cl=-65, Ca=+123, in muscle: Na=+65, K=-95, Cl=-90, Ca=+132

Review the concept of the electrical equivalent circuit model of the cell membrane potential

plasma membrane represents capacitors in parallel with conductors (open ion channels)


dysfunctional ion channels - autoimmune (Myasthenia gravis and neuromyotonia), nerve injury or after drug treatments or toxins that perturb cellular functions (marine toxins TTX, STX and ciguatoxin affect Na channels). Abnormal repolarization of Na channels cause ventricular arrhythmias; CNS disorders of excitability include episodic ataxias, familial hemiplegic migraines, dominantly inherited epilepsies

Ischemic Cerebral Edema

interruption to cerebral blood flow causes irreversible cellular damage due to cellular swelling - Cytotoxic edema, followed by vasogenic edema - blood vessels become permeable. Aquaporins are upregulated in animal models of stroke and water intoxication, around human brain tumors and can cause brain edema

Death by lethal injection

High concentration of potassium chloride which depolarizes excitable cells (nerve and muscle); cardiac muscle fails to generate action potentials because voltage gated sodium channels stay closed. Death is caused by heart failure

What is a graded potential

local response that has no threshold, may be hyperpolarization or depolarization, mediated by a receptor, amplitude is proportional to stimulus amplitude. Summation of responses occurs, spreads with decrement and fails to spread over long distances

Explain an action potential

propagated response with a threshold, evoked by depolarization ONLY, always overshoots 0mV, mediated by voltage gated channels, amplitude is independent of size of depolarization (all-or-none), no summation, amplitude is constant during propagation over long distances.

Explain how excitable cells convert stimuli into responses consisting of changes of conductance and membrane potential

membrane receptors mediate the conversion of the stimulus into local accumulation of positive charge in the stimulated region causes a change of Vm and conductance reflecting the conversion of stimulus into an electrical signal

Explain the concept of electrical signals spreading from their sites of origin with the decrement, governed by a length constant ()

stimulus to sensory ending of an afferent neuron produces local depolarization and adjacent regions (without the membrane receptors are also depolarized by the spreading of positive charge but less effectively and fade in size of the membrane potential as it spreads in both directions. The amplitude of the voltage signal fades out exponentially with increasing distance, length constant characterizes this exponential fall.

Relate the electrical properties of cable-like structures, such as axons and dendrites, to their length constants

higher the fiber diameter or resistance across a cells surface, higher the length constant

Review the signaling mechanisms giving graded responses in la afferent fibers in muscle spindles

When a muscle is stretched, groups of intrafusal muscle fibers within muscle spindles are stretched which stimulates mechanosensitive la afferent fiber wrapped around the central regions of these muscle fibers (monitors length), Golgi tendon organ is also stimulated (monitors tension). The muscle fibers have stretch -gated ion channels; mainly Na ions pass through and cause depolarization (if stimulus is large enough to reach threshold it will generate an impulse

Review the signaling mechanisms giving graded responses in la afferent fibers in rods in the retina

photons are absorbed by the visual pigment (rhodopsin) which activates a stimulatory G protein that increases breakdown of cGMP. Which causes Na ion channels to close and causes hyperpolarization of the rod (-40mV in dark, -56.7 in dark) - amplitude is dependent on light intensity, which means fall in cGMP is related to number of photons. Hyperpolarization spreads to secretory ending of the rod and causes reductions in transmitter released to neighboring bipolar cells in the retina

Review the signaling mechanisms giving graded responses in la afferent fibers in olfactory neurons in the nasal cavity

cilia on bipolar sensory neurons contain receptor proteins with binding sites for odorant molecules. Binding activates a G protein which causes a rise in adenylyl cyclase activity which leads to an increase in cAMP concentration which gates the opening of cation channels and causes entry of Na and Ca which results in depolarization (rise in Ca causes Cl channels to open and let out Cl ions). Amplitude increases with concentration of stimulating molecule. Cl concentration is very high and its leaving the cell aids in depolarization

Describe the all-or-none response to depolarization and the threshold for excitation

When current is large enough to shift the potential to threshold membrane potential, it excites the cell to fire an action potential (further increase in the magnitude of the depolarizing current pulse do not alter the amplitude of the impulse

Describe the physical features determining the trigger (spike-initiating) zone in neurons

in multipolar neurons the axon hillock is the initiating zone, in pseudounipolar and bipolar neurons, the impulse initiation zone is near the sensory endings, in skeletal muscle fibers the impulse zone is close to the central region that receives acetylcholine released by the motor neuron. ALL OF THESE ZONES HAVE A HIGH DENSITY OF VOLTAGE GATED NA+ CHANNELS


increase in muscle tone characterized by hyperexcitability of the stretch reflex with a decrease in reflex threshold. Hyperexcitability comes from abnormally increased activity of voltage gated sodium channels. Na channel blocking muscle relaxants are used to relieve these conditions


loss of olfactory sense from head injury that severs or compresses the axons of the olfactory neurons; if it lasts over a year it will be permanent; anosmia occurs in elderly because of degenerative loss of a fraction of the population of olfactory neurons; can also be congenital

Night Blindness

Rhodopsin is derived from Vitamin A in the diet; A deficiency will develop night blindness due to lack of rhodopsin. Rods are responsible for vision when light levels are low.

Describe the influence of the influx of sodium ions on the rising phase of the action potential

depolarization causes opening of voltage gated sodium channels in the membrane of the initiation zone, if it reaches threshold, the Na influx exceeds the efflux of K+ ions - this produces further depolarization, hence further opening of Na channels - drives the membrane towards E (Na)

Describe the influence of the efflux of potassium ions on the repolarizing phase of the action potential

depolarization induces the opening of voltage gated K+ channels - delayed kinetics - efflux of K+ will repolarize the membrane and cause the falling phase of the impulse -efflux of K drives potential towards E (K+) -> hyperpolarizing overshoot

Recognize the different time courses of changes in sodium and potassium conductances

K+ conductance has a slow activation and also closes more slowly, Sodium channels open quickly and when they reach their peak, they close quickly as well

Explain how the structural features of voltage gated sodium channels are related to the influence of depolarization on the closed and open states of this channel

charged component (segment 4) that acts as a voltage-sensing element for the channel protein, each subunit has a pore loop that endows the channel pore with its particular ion selectivity

Explain absolute refractory period

virtually all Na channels are inactivated, no stimulus can evoke an impulse

Explain relative refractory period

a new impulse can only be evoked by a larger stimulus, some Na channels are in the normal closed state and can be open, but a large number of K+ channels remain open and tend to oppose excitation of the axon

Summarize the locations of voltage gated channels in unmyelinated axons

uniform distribution (100 channels per square micrometer for both Na and K+ channels (much less than in nodes or ranvier in myelinated axons)

Summarize the locations of voltage gated channels in myelinated axons

lots of Na+ and K+ channels in axon initial segment, sodium channels are also found in presynaptic terminals and enriched in nodes of ranvier. Voltage gated K+ channels are mainly found at the paranodal and juxtaparanodal portions of both peripheral and central myelinated axons (maintain resting membrane potential of myelinated axon)

Explain how impulse conduction speed is related to fiber diameters of unmyelinated and myelinated axons

unmyelinated axons have small diameters that limit the effectiveness of current spread along the axon's interior (conduction velocity is about twice the fiber diameter), myelinated axons: depolarizing current takes finite time to drive membrane potential to threshold, regeneration of impulse at each node (no decrement - conduction velocity is six times fiber diameter

Describe how impulses are propagated in unmyelinated and myelinated axons

unmyelinated: continuous conduction, myelinated: saltatory conduction

Explain the advantages conferred by myelination

enhanced velocity of conduction because impulses generated only at nodes of ranvier about 1mm apart, large velocity is achieved in fibers with relatively small diameters, confining impulse to nodes means that Na loading during intense impulse traffic is minimized in myelinated axons, giving a huge energy saving

What are some ways that impulse conduction can be impaired

TTX, Saxitoxin, local anesthetics, demyelination

Tetradotoxin (TTX)

marine bacteria in Japanese puffer fish - binds to outside of Na channels and blocks sodium entry - impairs impulse conduction

Saxitoxin (STX)

red tide - blocks sodium entry externally and abolishes the impulse - numbness in 4-6 hours

How do local anesthetics impair impulse conduction

block Na channels at an intracellular site. Lidocaine and procaine - in uncharged form can cross the membrane, becomes charged and blocks Na Channel, block in the following order: small myelinated axons (A delta), unmyelinated axons (C fibers), then large unmyelinated axons (pain perception is A delta and C fibers)

How does demyelination impair impulse conduction

Na and K channels will be redistributed along the axon

How does demyelination cause decreased conduction velocity

frequency related block (failure to reach threshold), total conduction block and cross talk between axons

Multiple Sclerosis

demyelinating in the CNS - more common in women - oligodendrocytes are attacked by an autoimmune response. Problems with optic nerve/CN II, problems with muscle weakness (corticospinal tract), poor coordination with limb movements or balance, problems with speech (cerebellum)

Guillain-Barre Syndrome

autoimmune against Schwann cells - usually after respiratory or intestinal infection - ascending paralysis - life threatening when it reaches the diaphragm and other respiratory muscles

Chronic neuropathies

mutations produce heterogeneous dysmyelinating and demyelinating chronic neuropathies. Can be dominant or negative, can be congenital, can be adhesive proteins in Schwann cells and also axonal loss. Neurons have profound loss of myelination and may have never been myelinated (dysmyelination). Nerve conduction velocity is very slow.

Electrical synapses

gap junctions formed by 2 connexons (comprised of 6 units of four membrane spanning connexins), synchronized activity - hormone secreting cells in hypothalamus, some spinal cord motor neurons, pyramidal cells in hippocampus, mesencephalic nucleus between sensory neurons and retina between horizontal cells, between astrocytes, Schwann cells, cardiac cells, epithelial cells in a number of organs -> very fast transmission, unidirectional or bidirectional

Chemical synapses

neurotransmitters released by presynaptic cell (from active zones where exocytosis occurs) to bind to receptors on post synaptic cell membrane.

Axosomatic synapses

inhibitory action of the firing rate of postsynaptic neuron

Axodendritic synapses

excitatory action on firing rate of postsynaptic neuron

Axoaxonic synapses

inhibitory action on transmitter released by postsynaptic neuron

Tripartite synapses

pre-synaptic, post-synaptic neurons and astrocytes endfeet. Astrocytes modify neuronal transmission by transmitter release (e.g. glutamine) and transmitter uptake (e.g. glutamate)

Ionotropic receptors

proteins are also ion channels, binding causes channel opening (or closing) -> nicotinic AchR, GABA (A), NMDA (glutamate receptor)

Metabotropic receptors

G-protein-linked receptors influence enzymes to induce changes in second messengers in the post-synaptic cell -> muscarinic and adrenergic receptors

Synaptic delay

caused by many factors - time delay between arrival of impulse and onset of postsynaptic cell response

Describe how glutamate induces an EPSP by activation of ionotropic receptors which are cation channels

binds to NMDA, AMPA or kainate - cation channels allow influx of Na (NMDAR also Ca) and efflux of K ions. Evokes small depolarization called excitatory postsynaptic potential (EPSP) - fast depolarizing phase and slow repolarizing phase, amplitude reflects amount of glutamate released

Describe the ionic basis of the glutamate-induced EPSP

large influx of Na and small efflux of K - depolarization (falls far short of E (cation) because the number of channels opened is small)

Distinguish between the ionic bases of EPSPs induced by glutamate and IPSPs induced by glycine or GABA acting on their different ionotropic receptors

la afferents excite local interneurons via AMPA receptors - interneurons have inhibitory action by releasing glycine on motor neurons - impulse in interneuron evokes IPSP

Describe how EPSPs and IPSPs are integrated at the axon hillock and distinguish between spatial and temporal summation of synaptic potentials

initiation zone has lowest threshold for excitation -> integration site for synaptic potentials, spatial summation has additive effect (more than one impulse arrives at the same time), temporal summation also has additive effect (consecutive EPSPs/IPSPs happen before first can relax back to resting potential -> firing rate of a neuron is dictated by the combined effect of temporal and spatial summation

Cocaine as a local anesthetic

blocks sodium channels from inside - blocks transport proteins that produce re-uptake of dopamine, NE, and serotonin - prolongs their presence in synaptic clefts

Morphine administration

binds to enkephalin receptors on the C fiber terminal and acts as an agonist and reduces output of excitatory transmitters; C fiber terminals relay pain information to second order neurons in the spinal cord

Metabotropic and ionotropic receptors in diseases of nervous system

excessive activation, as well as inactivation has been shown to be associated with psychiatric, neurological and neurodegenerative diseases including Parkinson's, anxiety, depression, schizophrenia, pain and epilepsy. Use ionotropic glycine and GABA receptors as targets for treatments

Review the role of glutamate at synapses in the spinal cord involved in mediating the myotatic reflex

when a muscle is stretched, muscle spindles are excited which causes la afferent terminal to release glutamate which goes to the motor neuron AMPA receptors and excites them which causes agonist muscle to contract

Describe how local inhibitory interneurons, excited by la afferents, release glycine

la afferents excite inhibitory interneurons by glutamate and AMPA receptor, interneuron releases glycine onto motor neurons of the antagonist muscle -> reciprocal innervation causes agonist muscle to relax while agonist muscle contracts to cause myotatic reflex

Motor Unit

comprises of a motor neuron cell body, it's myelinated axon, the NMJs and the skeletal muscle fibers that it innervates

Motor nucleus

motor neurons innervating a muscle that have some cell bodies distributed over a few cord segments

The presynaptic terminal and boutons are covered by

Schwann cells without myelin

Review the notable features of transmission at the neuromuscular junction

every muscle fiber has only one excitatory synapse at its NMJ from one motor neuron ONLY; NMJ is where acetylcholine is released by exocytosis; every impulse in a motor neuron evokes an impulse in a muscle fiber; there are no inhibitory synapses in muscle fibers

List the steps in the life cycle of acetylcholine as a neurotransmitter

made by choline acyltransferase in the cytosol (good marker), degraded by AchE, choline is taken back up via cotransports with Na+ ions

Describe the microanatomy of the neuromuscular junction in relation to the function of transmission

active zones - sites of transmitter release where exocytosis occurs; voltage gated Ca channels nearby that stimulate vesicles to be released

Describe the structure of nicotinic Ach receptors at the muscle fiber end plate

has 5 subunits - 2abgd = fetal, 2abed = adult; adult permit larger currents but have more frequent opening times with shorter mean open time - better suited to fast activation of skeletal muscles

List the steps, after Ach is released, that must occur before the ionotropic nicotinic receptor functions as an open cation channel

diffusion across synaptic cleft -> 2 Ach molecules must bind to the ionotropic receptor -> conformational change occurs and channel opens -> allows influx of Na+ and efflux of K+ ions

Explain the ionic basis of the end plate potential

depolarizing effects of cation flux through open nAChRs spreads in both direction from the end plate with decrement (length constant)

Distinguish between the end plate potential and the muscle action potential

EPP can cause an action potential if it reaches threshold


block voltage gated Na channels and prevent arrival of impulse at nerve terminal and cause paralysis

Botulinum toxin

enters nerve terminal and interferes with docking of synaptic vesicles and inhibits exocytosis irreversibly - failure of Ach release causes paralysis. Can be used for reduction of saliva in Parkinson's, for pain relief, spasticity hemifacial spasm, focal dystonia


black widow spider venom - enters nerve terminal and interferes with exocytosis to promote massive irreversible release and depletion of Ach - initial contractions followed by paralysis


snail toxin - irreversible binding to voltage gated Ca channels in nerve terminal membrane - causes impaired calcium entry, low probability of exocytotic release of Ach -> flaccid paralysis

Physostigmine and neostigmine

reduce activity of AchE -> rise in Ach levels and prolongs its effect (reversible), used as a therapeutic agent

Malathion and parathion

insecticides IRREVERSIBLY bind to AchE and cause rise in Ach levels

Sarin and Tabun

nerve gases - IRREVERSIBLY reduce AchE and prolong Ach induced depolarization - cause death by paralyzing respiratory muscles

Carbachol, nicotine and succinylcholine

nicotinic agonists (nAChRs) - none of these are degraded by AchE in the cleft - prolonged binding and possibility of desensitization of the receptor

Curare, Pancuronium

nicotinic antagonists - reversible competitive (bind to nAChRs and compete with Ach)


snake venom - nicotinic antagonist - IRREVERSIBLY binds to Ach binding sites - paralysis


Ach antagonist at synapses in sympathetic ganglia to treat high blood pressure (superseded by better drugs)

Lambert-Eaton syndrome

autoimmune disease - muscle weakness due to antibodies against voltage gated Ca channels in motor nerve terminals - reduced number of channels gives impaired entry of Ca and poor release of Ach - failure of EPP to reach threshold

What are 2 treatments for LE syndrome

4-amino pyridine and neostigmine


blocks K channels and prolongs duration of impulses invading the nerve terminal. Prolonging depolarization enhances entry of calcium which facilitates release of Ach

Myasthenia gravis

auto immune disease with muscle weakness due to antibodies against nAChRs (reduced in number at the end plate), Ach release is normal but end plate membrane is less responsive - EPP fails frequently to reach threshold -> treat with neostigmine (give atropine to antagonize Ach's effects on cardiovascular system)

Depolarizing agents

cholinergic agonist - succinylcholine - short acting - not broken down by AchE but by plasma esterases, acts as agonist of Ach for nAChRs and causes long opening of cation channels - inactivates voltage gated Na channels - fibers become unexcitable

Non-depolarizing agents

reversible antagonists of nAChRs (curare and Pancuronium)

Tetanus toxin

exotoxin enters nerve endings of peripheral nerves and is transported by retrograde axonal transport to cell bodies - enters inhibitory interneurons and prevents normal release of inhibitory transmitter - hyperreflexia - both agonist and antagonist muscles experience stimulation

Strychnine poisoning

blocks glycine receptors in the CNS - same as tetanus toxin with spasms, convulsions and interference with breathing

Describe the sites of synthesis and storage of small molecule transmitters in nerve terminals

synthesized in the cytosol of nerve terminals and taken up into empty clear vesicles that will be tethered to the cytoskeleton

List the ionic mechanisms in the vesicular membrane that facilitate transmitter storage

filling of synaptic vesicles depends on established gradient of H+ ions - e.g. antiport exchanging Dopamine for H+

Review the roles of extracellular and intracellular calcium ions in transmitter release

calcium channels near active zones - calcium influx after AP causes rise in intracellular calcium concentration -> Ca2+ induces indirectly the phosphorylation of synapsin -> untethers synaptic vesicles from cytoskeleton and allows for fusion of the vesicle to the membrane

Review the steps in the process of exocytosis of neurotransmitter

MOBILIZATION - synapsin tethers to cytoskeleton and releases vesicle when phosphorylated -> TRAFFICKING - Rab proteins help move vesicle to active zone -> DOCKING - binding of vesicular snares (V-snare synaptobrevin and synaptotagmin) to nerve membrane snares (t-snare syntaxin and neurexin respectively) -> FUSION - synaptophysin forms fusion pore allowing transmitters to be released

Distinguish between the conditions necessary for release of small molecule transmitters and the co-release of these transmitters and neuropeptides

low nerve stimulation rates -> exocytosis of small clear vesicles due to local rise in Ca2+; high stimulation -> exocytosis of large dense core vesicles (neuropeptides) due to rise in Ca2+ spreading further

Describe the mechanisms for recycling of vesicular membrane following exocytosis

small neurotransmitters taken up by endocytosis in clathrin coated pits, clathrin falls off and fuses with endosome to form new vesicle to be refilled with transmitter. Neuropeptides taken up by endocytosis in clathrin pits, but transported back to soma to be refilled with propeptides by the retrograde axonal transport system (dynein)

Mini EPP's

small depolarizations due to release of one quantum -> quantal size (# of Neurotransmitters in one quantum)


packet of transmitter located in one synaptic vesicle

Quantal size

# of neurotransmitters in one quantum

Quantum content

# of quanta released by synaptic bouton under the influence of one invading impulse

Review the evidence for quantal release of transmitter and distinguish between quantum content and quantal size

quantum content can be estimated by (mean size of EPP/mean size of minEPP) - at the NMJ quantum content is 200 (200 vesicles/impulse), at other synapses mean quantum content is 1 (1 vesicle per impulse

Botulinum toxin

exotoxin acts as a protease - inactivates docking by breaking down synaptobrevin and prevents vesicular release of Ach IRREVERSIBLY - causes muscular weakness

Tetanus toxin

protease - enters PNS and passes into CNS via retrograde axonal transport - enters glycinergic interneurons and inactivates synaptobrevin and stops vesicular release of glycine IRREVERSIBLY - muscle spasms and interference with respiration - reverse with neuromuscular blocking agents and assisted ventilation


black widow spider toxin - depletes endings of cholinergic neurons - binds to neurexin/synaptotagmin complex and induces massive release of vesicular Ach -> irregular muscle spasm followed by flaccid paralysis

Neomycin and streptomycin

aminoglycoside antibiotics - inhibit exocytosis of Ach at motor nerve terminals - reversed competitively by raising extracellular calcium


K+ channel blocking drug prolongs duration of impulse, enhances Ca2+ entry to the motor nerve and raises probability of Ach release and hence quantum content

How do neurotransmitters alter quantal release

presynaptic inhibitory ending releases a transmitter at axoaxonic synapses - binds to receptors in the membrane of the second cell and reduces transmitter release (common on terminals of afferent neurons in the spinal cord


caused by hypoparathyroidism and causes tetany (spontaneous muscle contraction) and paresthesis due to repetitive firing of APs - in absence of Ca ions it is easier to open sodium channels and membrane is not as stable - leakiness causes depolarization; hypocalcemia also reduces transmitter release from vesicles

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