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27 Cards in this Set

  • Front
  • Back
What is a motor unit composed of?
single axon, which then results in many muscle fibers contracting
What is the difference between Weakness and Fatigue
Weakness is the loss of strength while fatigue is a time dependent weakness.

Example: You can have 20% muscle weakness constantly. You can have no muscle weakness, but do heavy lifting and become fatigued and unable to perform maximally
Non-eye Type I muscle (color, speed, mode)
white, fast, glycolytic
Non-eye Type II Muscle (color, speed, mode)
red, slow, oxidative
CMAP
recorded muscle potential that is a result of multiple motor units being stimulated resulting in increased force
What is the structure of the Neuromuscular Junction (3 structures)?
Presynaptic terminal, axon, and synapse. There is also a postsynaptic terminal
What does graded potential mean? Give some examples.
A graded potential is one that is time and concentration dependent. For example an EPP and pacemaking Sinoatrial Node are graded
What is a EPP (endpoint potential)?
An endpoint potential is a nonpropagated membrane depolarization
What is a MEPP?
Miniature Endpoint potential. This depolarization occurs by chance and releases some Ach
What are the properties of the neuromuscular junction
unidirectional, sensitive to drugs, signal delay, EPP, and amplification
What are the prejunctional events in the NMJ?
synthesis of ACh, packaging, vesicle supply and Ach release.
The Ach receptor binds how many ACh?
2
What happens to the choline in the synaptic cleft?
It gets recycled by transfer back into the presynaptic cleft. This can be inhibited by hemicholinium
What is the Na+Choline co-transport system?
This is what is used to reuptake choline into the presynaptic cleft.
How do we calculated the number of vesicles released from a NMJ?
N = Qr x p
Qr is the quantums released
p is the probability of release
What triggers the release of Ach into the NMJ?
Voltage-gated channels of the (L-type, lazy) allow Ca2+ to enter the nerve terminal

Ca2+ then triggers exocytosis of ACH
What are the two steps in the exocytosis of ACh into the NMJ?
First the vesicle docks with a docking protein and then releases its contents upon fusing
How is calcium removed from the presynaptic terminal?
This is done by a process of a Na+-Ca2+ exchanger, it is a slow process
What are the events in a synaptic cleft?
Diffusion of ACh, Binding of Ach to receptors (2 Ach/receptor), inactivation of ACh
What are the post-junctional events in NMJ?
Ion permeability change, the Na+/K+ channel which allows for EPP and muscle action
What is post-tetanic facilitation (PTF) as it relates to the NMJ?
A small amount of excess calcium accumulates in teh terminal, which makes a greater number of vesicles fuse, releasing more ACh and an amplified response.

However eventually too much stimuli will deplete Ach which will lead to failure to produce an AP
What can hinder ACh synthesis?
Cyanide, Choline deficiency, Hemicholinium
How can ACh transmission fail?
decrease EC Ca2+, Increase EC Mg2+, Botulinium Toxin, and Microtubular distrupting drugs
What is the difference between curare and alpha bungarotoxin?
Well they are both ACh receptor blockers.
Curare is a competitive inhibitor (reversible) while alpha bungarotoxin is irreversible
What two compounds can lead to persistant depolarization of the post-synaptic membrane and what does this mean?
Succinylcholine (reversible)
Decamethonium

This means that the membrane has been depolarized for so long that no further AP are created
What is the effect of marginal NMJ have on CMAP?
we see that there is a decremental response and that the post-tetanic potential worsens
What are two drugs/compounds that alter ACh destruction and what do they do?
Edrophonium (tensilon) is a reversible competitor that blocks AChE. It is useful in treating Myasthenia Gravis

DFP - diisofluorophosphate is irreversible and leads to systemic NMJ failure and paralysis (ACh remains in the NMJ... overstimulation)