1-36 Membrane Potential Flashcards
Membrane potential
difference in electral potential across cell membrane neurons: -70mV, RBS: -10mV Driven by K leak channels that allow K to flow and drive towards Ek (-95), but remains a little closer to positive by few Na leak channels that pull towards ENa (65) established by NA/K-ATPase: removes 3 Na+, Brings in 2 K+, hydrolyzes 1 ATP -> ADP + Pi measured by Foldman-Hodgkin-Katz equation: Em = RT/F * ln (Permeability K [K]out + etc + etc / Permeability K [K]in + etc + etc) etc for each ion of importance, usually K, Na, Cl (flip Cl cuz negative charge)
Equilibrium potential
membrane potential that is just sufficient to oppose the chemical potential for a specific ion so no net movement of that ion if channels were open Eion: RT/zF * ln([Ion]out/[Ion]in) Ek: -95 mV ENa: 65mV
Graded potentials
physiological stimuli can cause transient changes in membrane potential: graded potentials observed at jxns between neurons (synaptic potential) and neuron to NMJ (acetylcholic receptors, endplate potential) nervous systmem generally: graded potentials generated by stimulation NTreceptors (ligand gated ion channels), opens channel for cation to come in making the membrane less negative (depolized) or Cl- comes in and hyperpolarizes.
Types: Excitatory post-synaptic potential (EPSP) or IPSP
EPSP: activation of NTrecpet permable to Na+ or Ca+2, via ionotropic glutamate receptors
IPSP: activate NTR permable to Cl- summation happens at axon hillock: if reaches threshold potential will trigger action potential, _GABA receptors (_only adult neurons get hyperpolarized by Cl- because have mature low levels of Cl- so GABA drives Cl- in and drive Vm negative-er)
safety factor (thresholds)
degree that the EPSP generated at the NMJ exceeds the threshold required for AP firing
Action potential (neuronal)
dynamic, all or nothing, phasic change in membrane potential that can propagate along a neuron or surface of muscle cell
different form in different cel types (long/slow)
Events:
- EPSP summed with drifiting up to -50mV from baby influx on Na+
- Reach threshold and Depolarized: Voltage gated Na+ Channels open and Na+ rushes in
- Na+ channel conformational change and close: inactivation, remains inactive until membrane is repolaried* major reason for the refractory period (absolute OR relative)
- Repolarization: volatge gated K+ channels open in response to membrane depol by Na+ but are slower, K+ floods out of cell and often “overshoots” and causes hyperpolarization
- K+ channels eventually close and AP ends.
Jump along myelinated nerve axon via saltatory condution
Action potential (cardiac)
Cardiac action potential consists of four distinct phases (Figure 2a). In phase 0, upstroke occurs due to rapid transient influx of Na+. Later, Na+ channels are inactivated, combined with a transient efflux of K+. In phase 2, also known as the plateau phase, the efflux of K+ and the influx of Ca2+ are counterbalanced. At the end of the plateau, sustained repolarization occurs due to K+ efflux via the delayed rectifier K+ channels exceeding Ca2+ influx; this constitutes phase 3 of the action potential. Finally, as part of phase 4, resting potential in myocytes is maintained.