NMJ Flashcards by Erin Lee

somatic motor system control?

skeletal muscle via relayed output from the CNS

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where do UMNs start and synapse?

UMNs start in the brain → travel down the spinal cord → synapse on LMNs

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where do LMNs start and synapse?

LMNs exit the CNS → synapse on skeletal muscle fibers to cause contraction

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nmj?

Terminal of an LMN contacting a single skeletal muscle fiber

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Can one LMN innervate multiple muscle fibers?

yes

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How many NMJs does one muscle fiber have?

one NMJ per muscle fiber

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What type of synapse is the NMJ?

A chemical synapse with deep membrane invaginations on the muscle fiber

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What neurotransmitter do LMNs release?

acetylcholine

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What receptors are on the muscle fiber?

Nicotinic ACh receptors

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What enzyme terminates ACh activity at the NMJ?

Acetylcholinesterase

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Why does NMJ transmission always cause contraction?

Motor terminals contain thousands of vesicles and release excess ACh → always enough to reach threshold.

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Steps of synaptic transmission?

Action potential arrives at the presynaptic terminal

2.Voltage-gated Ca²⁺ channels open

Ca triggers vesicle fusion and neurotransmitter release.
NT diffuses and binds to postsynaptic receptors
NT is removed → transmission ends.

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What is the postsynaptic cell at the NMJ?

Skeletal muscle fiber

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What happens after ACh binds the receptor?

It is rapidly broken down by AChE

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What is the effect of blocking nAChRs (e.g., curare)?

Prevents muscle contraction → flaccid paralysis.

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What causes an end plate potential (EPP)?

ACh binds nicotinic receptors → Na⁺ influx → local depolarization of the muscle membrane.

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Is an EPP all-or-none or graded?

Graded potential

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What happens when the EPP reaches threshold?

Voltage-gated Na⁺ channels open → large Na⁺ influx → muscle action potential

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Do skeletal muscles need summation to fire an AP?

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What is the “high safety factor” at the NMJ?

LMNs release way more ACh than needed → every nerve AP reliably triggers muscle contraction

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Higher EPP amplitude →

higher frequency of muscle action potentials

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increased AP frequency in muscles leads to

stronger or sustained contractions

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AP spreads across the muscle fiber and down to what

T-tubules → contraction

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after ACh is used and broken down into choline, what happens?

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choline is taken back up into the neuron terminal and recycled to make more ACh

NMJ transmission is quickly terminated by which enzyme

AChE

role of AChE?

hydrolyzes ACh into choline and acetate into the synaptic cleft

Nicotinic ACh receptors are made up of

5 subunits

Why can only cations pass through nAChR

channel pores are negatively charged

If you block pre-synaptic VG calcium channels: Ca2+ entry? ACh release nAChR activation? end-plate potential action potential?

all will decrease decreased in amplitude for end-plate potential decreased in freq for action potential

If you block ACh release, what happens to: Ca2+ ACh release nAChR activation end-plate potential action potential

Ca2+ - no change ACh release - ↓ nAChR activation - ↓ end-plate potential - ↓ in amp action potential - ↓ in freq

If you over-activate ACh release, what happens to: Ca2+ ACh release nAChR activation end-plate potential action potential

Ca2+ - no change ACh release - ↑ nAChR activation - ↑ end-plate potential - ↑ action potential - ↑

If you block nAChR Activation, what happens to: Ca2+ ACh release nAChR activation end-plate potential action potential

Ca2+ - no change ACh release - no change nAChR activation - ↓ end-plate potential - ↓ action potential - ↓

If you over-activate nAChR, what happens to: Ca2+ ACh release nAChR activation end-plate potential action potential

Ca2+ - no change ACh release - no change nAChR activation - ↑ end-plate potential - ↑ action potential - ↑

If you block ACh removal, what happens to: Ca2+ ACh release nAChR activation end-plate potential action potential

Ca2+ - no change ACh release - no change nAChR activation - ↑ end-plate potential - ↑ action potential - ↑

If you over-activate ACh removal, what happens to: Ca2+ ACh release nAChR activation end-plate potential action potential

Ca2+ - no change ACh release - no change nAChR activation - ↓ end-plate potential - ↓ action potential - ↓

Infections from changes in NMJ

tetanus (tetanus toxin) botulinum (botulinum toxin) cyanobacteria (anatoxin)

toxins from changes in NMJ

plant - poison hemlock animal - a-latrotoxin chemical - organophosphates

diseases from changes in NMJ

myasthenia gravis lambert-eaton myasthenia

drugs for changes in NMJ

AChE inhibitors (physostigmine) nAChR blockers (pancuronium)

Botulism is caused by

botulism toxin

which species are most sensitive to botulism?

horses and wildfowls

symptom of botulism

progressive flaccid paralysis in all limbs (tetraparesis) dysphagia death from respiratory failure

dysphagia?

inability to eat

botulism toxin is produced by which bacteria?

gram+, anaerobic bacterium = Clostridium botulism

does botulism affect the muscles themselves?

No; toxin only attacks the NMJ

is botulism potent?

Yes; lethal dose is really low

botulism targets the pre or post synaptic motor neuron of the NMJ

pre-synaptic motor neuron

mechanism of botulism

inhibits ACh release by digesting SNARE proteins → No signal released → No contraction

organophophates used for

pesticides and some anthelminitics

which chemical is the major cause of animal poisioning?

Organophosphates

symptoms of Organophosphates?

muscle spasms and weakness respiratory distress death due to respiratory muscle paralysis

mechanism of organophosphates

irreversibly inhibit AChE → prevent breakdown → overstimulation of muscle fiber

T/F Myasthenia Gravis is common form of muscle weakness in both cats and dogs

TREU

two forms of myasthenia gravis?

congenital and acquired

mechanism of acquired myasthenia gravis?

autoimmune disease where antibodies are against the nAChRs at the NMJ

symptoms of myasthenia gravis

general muscle weakness difficulty swallowing megaesophagus

mechianism of myasthenia gravis

blocks ACh binding → reduce Na+ influx → lowers the end-plate potential below the threshold → no AP → no contraction

for myasthenia gravis, antibodies get stuck at the receptors. how does this affect the channels?

antibodies are stuck at the receptors → cross-linking two receptors → internalization and degradation → reduce # of functional nAChRs on the muscle membrane

NMJ Flashcards

(58 cards)