Lecture 4 The Action Potential

Thus vg na channel inactivation mediates absolute

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thus, vg-Na+ channel inactivation mediates “absolute refractory period” b/c need to return to RMP to remove and this limits the maximal rate of firing. Closure of sodium channels. Vg-Na+ channels: Blockade (chemically blocking) produces “reversible lesion” by preventing depolarization results in blockade of action potentials i.e. no rising phase is possible. e.g. tetrodotoxin (TTX) from pufferfish or fugu also site of action for local aneasthetics sodim channel blocker Vg-K+ channels delayed (rectifying) voltage-gated K+ channels four polypeptides four subunits 6 transmembrane spans/domains voltage-sensitive slow activation selective pore Vg-K+ channel also slow to close which mediates “relative refactory period” i.e.
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higher than “at rest” K+ permeability therefore need greater generator potential for AP selective pore as for non-gated K+ channel similar vg mechanism as vg Na+ channels ion channels during AP Rest: ng-K+ open vg-Na+ closed vg-K+ closed Rise: ng-K+ open vg-Na+ open vg-K+ closed Fall ng-K+ open vg-Na+ inactivated vg-k+ open Rest ng-K+ open vg-Na+ reset/closed vg-K+ closed inactivation is key critical for spatial aspects of the AP: conduction from one place to another Conduction – mvmt of AP from place to place along the membrane AP generation in the axon hillock AP down the axon conduction velocity and myelination Generation of AP in axon hillock axon hillock (initial segment) high in vg Na+ channels high sensitivity (relative to dendrites & cell body) to “generator potentials” amplifies generator potential positive feedback relation – generator potential reaches axon hillock → decreased membrane potential (depolarization) → opening of vg-Na+ channels in membrane → increased Na+ permeability → increased flow of Na+ into cell – > decreased membrane potential (depolarization) act like a “domino effect” generation and conduction of APs density of voltage-gated Na+ channels determines sensitivity to depolarization
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