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WEEK 6:

Action Potentials:

QuestionAnswer
depolarise membrane potential becomes positive inside due to influx of Na+ ions through voltage gated Na+ channels
repolarise membrane potential goes back to resting potential (-70mV) when voltage gated K+ channels open and K+ leave
hyperpolarise membrane potential goes more negative than resting potential (-70mV)
refractory period time after AP when neuron cannot fire another AP
passive conduction ensures adjacent membrane depolarises so AP travels down axon
what is nerve conduction affected by axon diameter, myelination and temperature
how does axon diameter affect nerve conduction bigger diameter = more nerve conduction velocity as less resistance
how does myelination affect nerve conduction saltatory conduction
all of nothing principle need to fire at full strength or else will not pass threshold to generate AP
stages of AP stimulus -> resting potential (-70mV) increases due to depolarisation (Na+ channels open), repolarisation (Na+ channels close and K+ channels open), hyperpolarisation (too much K+ out), return to resting potential
potential at resting potential and repolarisation -70mV
potential at depolarisation +50mV
potential at hyperpolarisation -90mV
AP upstroke fast positive feedback where stimuli causes membrane depolarisation (increase Na+ permeability + Na+ channels open) leading to increased Na+ influx making membrane more positive
AP downstroke slow negative feedback where membrane depolarisation (increase positivity) which increases K+ permeability (K+ channels open) increasing K+ outflow so the membrane hyperpolarises (becomes negative; back to resting potential)
Na+ is the ion responsible for AP upstroke in neurons, skeletal muscle, cardiac muscle
Ca2+ is the ion responsible for AP upstroke in cardiac muscle, smooth muscle and endocrine cells
describe how Ca2+ and Na+ is responsible for AP upstroke in cardiac muscle Na+ used for rapid propagation and Ca2+ is used for contraction
Created by: kablooey
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