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27 Cards in this Set
- Front
- Back
What is a motor unit composed of?
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single axon, which then results in many muscle fibers contracting
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What is the difference between Weakness and Fatigue
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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 |
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Non-eye Type I muscle (color, speed, mode)
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white, fast, glycolytic
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Non-eye Type II Muscle (color, speed, mode)
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red, slow, oxidative
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CMAP
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recorded muscle potential that is a result of multiple motor units being stimulated resulting in increased force
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What is the structure of the Neuromuscular Junction (3 structures)?
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Presynaptic terminal, axon, and synapse. There is also a postsynaptic terminal
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What does graded potential mean? Give some examples.
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A graded potential is one that is time and concentration dependent. For example an EPP and pacemaking Sinoatrial Node are graded
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What is a EPP (endpoint potential)?
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An endpoint potential is a nonpropagated membrane depolarization
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What is a MEPP?
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Miniature Endpoint potential. This depolarization occurs by chance and releases some Ach
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What are the properties of the neuromuscular junction
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unidirectional, sensitive to drugs, signal delay, EPP, and amplification
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What are the prejunctional events in the NMJ?
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synthesis of ACh, packaging, vesicle supply and Ach release.
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The Ach receptor binds how many ACh?
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2
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What happens to the choline in the synaptic cleft?
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It gets recycled by transfer back into the presynaptic cleft. This can be inhibited by hemicholinium
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What is the Na+Choline co-transport system?
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This is what is used to reuptake choline into the presynaptic cleft.
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How do we calculated the number of vesicles released from a NMJ?
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N = Qr x p
Qr is the quantums released p is the probability of release |
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What triggers the release of Ach into the NMJ?
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Voltage-gated channels of the (L-type, lazy) allow Ca2+ to enter the nerve terminal
Ca2+ then triggers exocytosis of ACH |
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What are the two steps in the exocytosis of ACh into the NMJ?
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First the vesicle docks with a docking protein and then releases its contents upon fusing
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How is calcium removed from the presynaptic terminal?
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This is done by a process of a Na+-Ca2+ exchanger, it is a slow process
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What are the events in a synaptic cleft?
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Diffusion of ACh, Binding of Ach to receptors (2 Ach/receptor), inactivation of ACh
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What are the post-junctional events in NMJ?
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Ion permeability change, the Na+/K+ channel which allows for EPP and muscle action
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What is post-tetanic facilitation (PTF) as it relates to the NMJ?
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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 |
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What can hinder ACh synthesis?
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Cyanide, Choline deficiency, Hemicholinium
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How can ACh transmission fail?
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decrease EC Ca2+, Increase EC Mg2+, Botulinium Toxin, and Microtubular distrupting drugs
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What is the difference between curare and alpha bungarotoxin?
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Well they are both ACh receptor blockers.
Curare is a competitive inhibitor (reversible) while alpha bungarotoxin is irreversible |
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What two compounds can lead to persistant depolarization of the post-synaptic membrane and what does this mean?
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Succinylcholine (reversible)
Decamethonium This means that the membrane has been depolarized for so long that no further AP are created |
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What is the effect of marginal NMJ have on CMAP?
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we see that there is a decremental response and that the post-tetanic potential worsens
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What are two drugs/compounds that alter ACh destruction and what do they do?
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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) |