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Flashcards in Rotation: Synaptic Phys Deck (17):

What is the average MEPP amplitude?



1. Describe the mechanisms by which curare and elevated Mg/low Ca solutions produced their effects.

  • Curare = nicotinic receptor antagonist (non-depolarizing) --> flaccid paralysis
  • Elevated Mg/low Ca = mimic of curare action bc no Ca++ available --> no vesicle exocytosis --> flaccid paralysis


In the heart, ACh is _____ but in muscle it is ____.

heart = inhibitory; muscle = excitatory


8. Differentiate between spontaneous miniature end plate potentials (MEPPs) and nerve‐evoked end plate potentials (EPPs).

  • MEPPs = small depolarizations NOT caused by NTs binding after an AP, but by spontaneous release of 1 vesicle/quanta - "incontinence"
  • EPPs = depolarizations of skeletal muscle fibers caused by NTs binding to the postsynaptic membrane after an AP caused their release


3. Describe the main experimental observations that underlie the Quantum Hypothesis of transmitter secretion.

  • states that transmitter is released from presynaptic nerve terminals solely in transmitter packages (quanta)
  • proof = MEPS exist and are always the same amplitude


If the low Ca++ preparation is stimulated at high frequency, _____ and can be sufficient enough to allow muscle contraction.



Curare acts by blocking ACh receptors on the ____ side.



5. Recognize the effects of neostigmine on synaptic transmission, and describe the drug’s mechanism of action.

  • neostigmine = AChEI blocks AChE active site
  • does not cross BBB
  • used to treat MG
  • antidote for curare poisoning


The muscarinic receptor is a _____ receptor.



Tetanus blocks the inhibitory signals from a motor neuron. What results?

over firing at the NMJ--> tetanic spasms


2. Recognize and understand the events that underlie the visually‐observed transition from individual muscle twitches to a tetanus as the frequency of stimulation to the motor nerve is increased.

tetanic state = motor unit maximally stimulated by motor neuron via multiple impulses at high frequency Increased freq. of stimulation --> increased depolarization/muscle contraction twitches--> facilitation due to Ca++ remaining--> twitches begin to overlap b/c there's not enough time for relaxation


What happens when too much neostigmine is given?

Bc it is structurally similar to ACh, it can interact with the AChR to antagonize its beneficial effects


6. Describe synaptic facilitation and synaptic depression and how they interact during repetitive stimulation in curare and in elevated Mg/low Ca solutions.

  • facilitation = Ca++ build up in pre-synaptic terminal--> more NT vesicle exocytosis

- helps overcome curare effects

  • depression = depletion of NT vesicles


Do MEPPs persist under low Ca++ conditions?



7. Describe the causes of myasthenia gravis and the myasthenic syndrome, and the effects of these diseases on synaptic transmission at the neuromuscular junction.

  • MG= antibodies to AChR (postsynaptic) --> weakness that is worse w/ exertion
    • Tx: pyridostigmine
  • myasthenic syndrome = antibodies to Ca++ channels (presynaptic)--> weakness that improves w/ exercise (facilitation)
    • AKA Lambert-Eaton Syndrome
    • assoc w/ small cell lung CA
    • Tx: pyridostigmine


What was the difference btw the low Ca++ preparation and the curare prep?

curare was much slower to exert its paralytic action


What does too much ACh lead to?

SLUDGE symptoms in PNS