Smith: Neuromuscular Junction Flashcards Preview

Block 5 Week 1 Meg > Smith: Neuromuscular Junction > Flashcards

Flashcards in Smith: Neuromuscular Junction Deck (37):
1

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

Sherrington's law;
tendon reflex - excited extensor and inhibits flexor

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.

relaxes

3

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

glycine

4

What blocks glycine?

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

5

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

Renshaw cells

6

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

motor unit

7

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

end plate potential
action potential
**have different mechanisms

8

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

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

9

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

Curare

10

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

Na+

11

What is an MEPP?

miniature end plate potentials

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.

True

13

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

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

14

What gets rid of released ACh?

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

15

What forms up ACh?

acetate and choline

16

What happens if you block AChE?

lots of ACh at neuromuscular junction!!!

17

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

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

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

T-tubule; ryanodine; troponin

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+?

T-tubules

20

What are some organophosphates? How do they work?

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

21

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

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

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?

alpha-bungarotoxin

23

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

Mg++

24

What toxins prevent release of quanta at the neuromuscular junction?

botulinum
tetanus toxin

25

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

depletion **dumps ACh

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.

Lambert-Eaton myasthenic syndrome (LEMS)

27

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

MEPPs are not Ca+ dependent - they fire spontaneously

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.

myasthenia gravis

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.

nicotinic

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.

Botulinum and Tetanus toxin

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.

botulism

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.

Tetanus

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.

inhibitory neurotransmitters; hyper-excitation

34

How does botulism differ from tetanus?

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.

35

What is the synaptic effect of botulinum toxin?
What is the synaptic effect of tetanus?

inhibits ACh release in NMJs;
inhibits glycine and GABA release in CNS

36

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

flaccid; spastic

37

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

glycine
GABA