Synaptic Transmission Lab Flashcards

1
Q

Why do individual MEPP’s vary substantially in amplitude?

A

The reason that there’s variation in the amplitude of EPSPs is biological variation. Not all vesicles are the same size or contain the same number of neurotransmitter molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does a notch or inflection of the AP rising phase reflect?

A

This is depolarization of the cell via opening of ACh sodium channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Did the electrode come out of the cell? If so, why?

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

signs/symptoms of botulism

A

FLACCID paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MOA of botulism

A

inhibits vesicle fusion with presynaptic membrane by cleaving synaptobrevin (SNARE protein).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of botulism

A

1) in infants often caused by honey 2) most commonly canned foods 3) wounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment for botulism

A

antitoxin and supportive care. may need to be on a ventilator.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why is botulism relatively more common in Colorado, compared to other places?

A

more home canning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Can you observe discreet “steps” in the amplitudes of successive EPP’s?

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are the “steps” about the size of a MEPP?

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

signs/symptoms of myasthenic syndrome

A

weakness of legs and arms. leg involvement usually more severe than in MG. proximal muscle weakness. respiratory muscle weakness. similar to MG presentation but eye signs are much more PROMINENT in MG. Distinct characteristic is that with muscle use, REFLEX STRENGTH INCREASES.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MOA of myasthenic syndrome

A

auto-antibodies block presynaptic voltage-gated calcium channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

causes of myasthenic syndrome

A

1) usually paraneoplastic syndrome associated with lung cancer. 2) may also be associated with autoimmune diseases (eg. hypothyroidism/DM type 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treatment for myasthenic syndrome

A

1) if paraneoplastic treatment with chemo or radiation usually leads to resolution of symptoms. 2) you can also improve symptoms with pyridostigmine. 3) if autoimmune IVIG and plasma exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mg/Low Ca solution – why is evoked but not spontaneous release affected by this solution?

A

spontaneous release isn’t dependent on calcium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does high frequency stimulation in the Mg/Low Ca solution allow muscle contraction?

A

facilitation due to increase in intracellular calcium ion concentration.

17
Q

How does Mg/Low Ca solution work?

A

produces a presynaptic block, similar to myasthenic syndrome, by reducing transmitter release.

18
Q

Why does the muscle begin to twitch when the curare solution is first added?

A

Curare just hasn’t had time to act yet.

19
Q

EPP

A

nerve-evoked end plate potential.

20
Q

MEPP

A

miniature end plate potentials.

21
Q

What would be the effect of a therapeutic dose of neostigmine on a normal person?

A

Probably wouldn’t have much of an effect because you normally have an excess of ACh.

22
Q

effect of neostigmine overdose? MOA of effect?

A

DUMBBELS

23
Q

signs/symptoms of botulism?

A

usually starts with cranial muscle weakness, ANS signs including dry mouth/constipation/postural hypotension, difficulty talking and nausea, vomiting. classic triad of bulbar palsy + descending paralysis + clear senses and mental status. NO fever.

24
Q

differentiate between spontaneous end plate potentials (MEPPs) and nerve-evokd end plate potentials EPPs)

A

MEPPs are spontaneous depolarizations of the postsynaptic membrane from a single vesicle. EPPs result from an AP in the presynaptic cell releasing neurotransmitters that bind to ACh receptors and depolarize the membrane.

25
Q

what is the mechanism at play in repetitive stimulation in curare?

A

depression

26
Q

what is the mechanism at play in elevated Mg/low Ca solutions?

A

facilitation