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18 Cards in this Set
- Front
- Back
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in a passive membrane what is the relationship between Em & Im?
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- Em linear function of Im
- aka if Im is 2x then Em is 2x more depolarized |
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in a passive membrane, local changes in Em generate what?
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- local depolarizations
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what channels generate active membranes?
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- VG channels
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below the threshold the membrane behaves like a ______ membrane. What is the depolarization due to? repolarization/hyperpolarization?
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- passive
- VG sodium, VG potassium |
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what happens to depolarization if you lower the concentration of sodium outside the cell? repolarization?
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- slower rate of rise
- smaller depolarization - nothing occurs to repolarization |
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what happens to repolarization if you raise the concnetration of K outside the cell? depolarization?
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- less depolarization occurs @ slower rate
- nothing happens to depolarization |
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what segment of the Na channel has the + charges? forms the pore? What about K channel?
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- S4 - positive charges
- p loop forms the pores - K channel is made from 4 different genes - S4 is still the positive segment |
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What is the difference between K & Na channels in terms of opening once they are stimulated? How does this explain the AP?
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- Na channels open very rapidly but then inactivate
- K channels are more sluggish but can reopen & close - explains AP because sodium channels more sensitive to changes in membrane potential so depolarize fast then inactivate & K channels are more sluggish and do not inactivate |
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what 2 things drive the membrane back down after depolarization?
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- inactivation of Na channels & activation of K channels
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___ channels are more sensitive to voltage, open more rapidly and inactivate
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- Na
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do ion concentrations change following one or several action potentials?
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NO
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what is hyperkalemic periodic paralysis? where is Erest? what is the pathogenesis with elevated K & Na channel mutations?
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- occurs while resting after working out, appears in childhood, attacks last 1-2 hours
- Erest is higher than normal, there is high extracellular potassium - mutations in the sodium channel cause this - higher extracellular potassium causes depolarization of the aberrant Na channels - get stuck in activated state & therefore membrane remains depolarized & other WT Na channels inactivate |
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What two ions are involved int he plateau phase of the cardiac AP?
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- calcium & potassium - calcium trying to keep cell depolarized - they slowly inactivate & K channels will repolarize
- interesting is that calcium [ ] actually changes during this time |
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What happens in multiple schlerosis?
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- demyelination exposes leaky membrane that shunts regenerative current & blocks AP conduction
- no Na+ channels exposed membrane, it is unable to regenerate the in- ward current necessary for continued action potential generation and action potential conduction fails |
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What happens during APs in skeletal muscle?
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- skeletal muscle activates VG calcium channels
- they activate another channel on SR receptor that is not VG - called a ryanidine receptor - this is what really raises Ca levels in skeletal muscle |
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what happens during APs at a nerve terminal?
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- VG Ca channels open up causing depolarization & fusion of vesicles with NT
- NT diffuses across the synaptic cleft & causes depolarization on the other side of cell |
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absolute refractory period
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- due to inactivation of Na channels - no matter how big the stimulus you cannot fire another AP
- sets upper limit for AP firing |
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relative refractory period? also what happens to the amplitude of the new AP?
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- VG K channels are still open therefore elevated K permeability makes it harder to fire another AP
- in order to fire another one you need to open up enough Na channels - big enough stimulus - amplitude of new AP is decreased |
