Synaptic Transmission Lab Flashcards
Why do individual MEPP’s vary substantially in amplitude?
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.
What does a notch or inflection of the AP rising phase reflect?
This is depolarization of the cell via opening of ACh sodium channels.
Did the electrode come out of the cell? If so, why?
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signs/symptoms of botulism
FLACCID paralysis.
MOA of botulism
inhibits vesicle fusion with presynaptic membrane by cleaving synaptobrevin (SNARE protein).
Causes of botulism
1) in infants often caused by honey 2) most commonly canned foods 3) wounds
Treatment for botulism
antitoxin and supportive care. may need to be on a ventilator.
Why is botulism relatively more common in Colorado, compared to other places?
more home canning
Can you observe discreet “steps” in the amplitudes of successive EPP’s?
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Are the “steps” about the size of a MEPP?
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signs/symptoms of myasthenic syndrome
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.
MOA of myasthenic syndrome
auto-antibodies block presynaptic voltage-gated calcium channels.
causes of myasthenic syndrome
1) usually paraneoplastic syndrome associated with lung cancer. 2) may also be associated with autoimmune diseases (eg. hypothyroidism/DM type 1)
Treatment for myasthenic syndrome
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
Mg/Low Ca solution – why is evoked but not spontaneous release affected by this solution?
spontaneous release isn’t dependent on calcium.
Why does high frequency stimulation in the Mg/Low Ca solution allow muscle contraction?
facilitation due to increase in intracellular calcium ion concentration.
How does Mg/Low Ca solution work?
produces a presynaptic block, similar to myasthenic syndrome, by reducing transmitter release.
Why does the muscle begin to twitch when the curare solution is first added?
Curare just hasn’t had time to act yet.
EPP
nerve-evoked end plate potential.
MEPP
miniature end plate potentials.
What would be the effect of a therapeutic dose of neostigmine on a normal person?
Probably wouldn’t have much of an effect because you normally have an excess of ACh.
effect of neostigmine overdose? MOA of effect?
DUMBBELS
signs/symptoms of botulism?
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.
differentiate between spontaneous end plate potentials (MEPPs) and nerve-evokd end plate potentials EPPs)
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.
