Q__________Post valentine Action potential=====q28 - miracoli

[ArchivalUser]

A 55-yrs-old man sees a neurologist because of weakness in his legs that improves over the course of
the day or with exercise. Extracellular electrical recordings from a single skeletal muscle fiber reveal normal miniature end-plate potentials. Low-frequency electrical stimulation of the motor neuron, however, elicits an abnormally small depolarization of the muscle fibers. The amplitude of the depolarization is increased after exercise.The molecular mechanism underlying these symptoms is most similar to which of the following?
A) Acetylcholine
B) Botulinum toxin
C) Curare
D) Neostigmine
E) Tetrodotoxin

[ArchivalUser]

E..

[ArchivalUser]

??

[ArchivalUser]

BB

Botulinum inhibits release AcCh. Tetrodotoxin acts by blocking Na channels.

[ArchivalUser]

Botulinum toxin

[ArchivalUser]

Yes it is B..
I overthought Like the molecular mechanism is channel blocking action and both the Ab and tetrodotoxin block the channel.
But yes Botulinum is more sensible.

[ArchivalUser]

BB is correct
-Lambert-Eaton myasthenic syndrome(LEMS) and botulism cause Dysfunction in quantal Ca-mediated synaptic vesicle release mechanism to produce EPP but no effect on MEPP (because a synaptic vesicle can be releases SPONTANEOUSLY, without Calcium mediated, and produce MEPP)
- Botulinum toxin inhibits muscle contraction presynaptically by decreasing the amount of ACh
released into the neuromuscular junction. In contrast, curare acts post-synaptically, blocking the
nicotinic ACh receptors and preventing the excitation of the muscle cell membrane.
-Tetrodotoxin blocks voltage-sensitive Na+ channels, impacting both the initiation and the propagation of action
potentials in the motor neuron. Both ACh and neostigmine stimulate muscle contraction.


Thank you for participation
For more explanation about membrane potential check here
http://www.usmleforum.com/showthread.php?tid=767949