Smith: Neuromuscular Junction

Question 1

When one set of muscles is stimulated, muscles opposing their action are inhibited. Give an example of this.

Answer 1

Sherrington’s law;

tendon reflex - excited extensor and inhibits flexor

Question 2

Sherrington’s law of reciprocal innervation states that: When a muscle contracts, it’s direct antagonist (blank) to an equal extent allowing smooth movement.

Answer 2

relaxes

Question 3

Renshaw cells release (blank) which causes an inhibitory postsynaptic potential in the motor neurons. This allows motor neurons to avoid continuing to discharge.

Answer 3

glycine

Question 4

What blocks glycine?

Answer 4

strychnine **causes muscular convulsions and eventually death through ashpyxia or sheer exhaustion

Question 5

(blank) are also the target of the toxin of Clostridium tetani, a spore-forming anaerobic bacterium that lives in the soil.

Answer 5

Renshaw cells

Question 6

The amount of fibers that one motor neuron synapses is called a (blank)

Answer 6

motor unit

Question 7

What are the two components of the electrical event that occurs when a nerve is stimulated at the neuromuscular junction?

Answer 7

end plate potential
action potential
**have different mechanisms

Question 8

T/F: In skeletal muscle, the end plate potential always reaches threshold to fire an action potential. It is always supra-threshold.

Answer 8

True

**this is called the safety factor of the neuromuscular junction

Question 9

What binds to ACh receptors on post-synaptic membrane of muscle cells and reduces the end plate potential?

Answer 9

Curare

Question 10

In a ligand-gated ion channel, ACh binds to the channel, and allows for (blank) to pass inside the cell.

Answer 10

Na+

Question 11

What is an MEPP?

Answer 11

miniature end plate potentials

Question 12

T/F: End plate potential is built up of small all-or-none quanta which are identical in size and shape with the spontaneous occurring miniature potentials.

Answer 12

True

Question 13

What are the individual MEPP potentials most likely due to? What is the end plate potential most likely due to?

Answer 13

the release of 1 vesicle of ACh; the release of multiple vesicles

Question 14

What gets rid of released ACh?

Answer 14

AChE (acetylcholineesterase) which breaks down ACh to acetate and choline. The choline will be recycled back via a choline transporter.

Question 15

What forms up ACh?

Answer 15

acetate and choline

Question 16

What happens if you block AChE?

Answer 16

lots of ACh at neuromuscular junction!!!

Question 17

What’s the effect of blocking AChE on spontaneous MEPPs?

Answer 17

end plate potentials are larger and their duration is longer, but their frequency is the same
**the time course of the end plate potentials is dependent on how long the neurotransmitter is present in the junction

Question 18

Na+ action potential depolarizes (blank) membrane
This depolarization causes voltage sensitive dyhidropyridine receptors (Ca2+ channels) to change conformation of (blank) receptors
Ca2+ is released from ryanodine sensitive stores
Released Ca2+ binds to (blank), revealing cross-bridge biding sites on actin molecules

Answer 18

T-tubule; ryanodine; troponin

Question 19

How does Ca+ get into the belly of the muscle and open up the DHP receptors to allow for lots of release of Ca+?

Answer 19

T-tubules

Question 20

What are some organophosphates? How do they work?

Answer 20

insecticides and nerve gases; block AChE **don’t function at the neuromuscular junction, really - more-so on smooth muscle

Question 21

Nerve gases cause ACh to build up. What does this lead to?

Answer 21

runny nose
bronchial secretions
tight chest
dim vision
pin-point pupils
drooling
perspiring
nausea
vomiting

Question 22

What is the Cobra toxin that binds to the ACh receptor at the neuromuscular junction and blocks the activating of the muscle, leading to muscle paralysis?

Answer 22

alpha-bungarotoxin

Question 23

What ion in excess can interfere with Ca+ mediated release of quanta?

Answer 23

Mg++

Question 24

What toxins prevent release of quanta at the neuromuscular junction?

Answer 24

botulinum

tetanus toxin

Question 25

Black widow spider venom causes a complete (blank) of acetylcholine, leading to initial spasm and then paralysis

Answer 25

depletion **dumps ACh

Question 26

An autoimmune disease affecting presynaptic Ca2+ channels; produces an antibody that binds to the presynaptic Ca+ channels at the neuromuscular junction, so there is a loss of ligand-gated ion channels, and this reduces the release of ACh.

Answer 26

Lambert-Eaton myasthenic syndrome (LEMS)

Question 27

Why are EPPs reduced, but the amplitude of MEPPs are normal in LEMS?

Answer 27

MEPPs are not Ca+ dependent - they fire spontaneously

Question 28

Autoimmune Diseases affecting nicotinic ACh receptors. Muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected.

Answer 28

myasthenia gravis

Question 29

In myasthenia gravis, antibodies bind to (blank) receptors, which causes receptor internalization. This causes fatigue of muscles, because there are not enough (blank) receptors. There is also a loss of junctional folds.

Answer 29

nicotinic

Question 30

These toxins act by cleaving snare proteins involved in fusion of synaptic vesicles with the presynaptic membrane - this paralyzes these muscles and gives a vacant expression without wrinkles.

Answer 30

Botulinum and Tetanus toxin

Question 31

Caused by consuming food containing Clostridium bacteria or by infection of wounds by spores.
Can cause paralysis at peripheral neuromuscular synapses due to the reduction of ACh release and therefore weak muscular contractions.
Produces neuromuscular weakness.
Extreme cases respiratory failure due to paralysis of diaphragm.

Answer 31

botulism

Question 32

Typically results from contamination of puncture wounds by Clostridium tetani bacteria that produce tetanus toxin. Often found in soil contaminated with manure, and animal and human feces (It is not transmitted from person to person).
Tetanus has also been associated with clean wounds, surgical procedures, insect bites, dental infections, and intravenous drug use.

Answer 32

Tetanus

Question 33

Tetanus blocks release of (blank) from interneurons, e.g.Renshaw cells.
Loss of synaptic inhibition on spinal  motorneurons.
Results in (blank) of skeletal muscle and tetanic contraction, leading to Lockjaw.

Answer 33

inhibitory neurotransmitters; hyper-excitation

Question 34

How does botulism differ from tetanus?

Answer 34

In botulism, ACh receptors are blocked, so that muscles are paralyzed (botox). In tetanus, inhibitory neurotransmitters cannot be released, so this causes hyper-excitation and contraction of skeletal muscles, particularly in the jaw.

Question 35

What is the synaptic effect of botulinum toxin?

What is the synaptic effect of tetanus?

Answer 35

inhibits ACh release in NMJs;

inhibits glycine and GABA release in CNS

Question 36

What type of paralysis is caused by the botulinum toxin? What type of paralysis is caused by the tetanus toxin?

Answer 36

flaccid; spastic

Question 37

Tetanus toxin inhibits CNS interneuronal synapses that release inhibitory transmitters, (blank) and (blank)

Answer 37

glycine

GABA