Membrane potential depolarization

We have found that the communication between Ca2+ sparks and BK channels can be tuned by membrane potential (this study, Herrera et al 2001) and by the accessory / subunit (Brenner et al 2000, Petkov et al 2001). This effect can be accounted for based on the allosteric relationship between the BK channel voltage and Ca2+ sensors, whereby membrane potential depolarization favours a channel conformation that has a higher Ca2+ sensitivity. The /b subunit has a similar role to increase the apparent Ca2+ sensitivity of the a subunit. 

The process starts with the opening of voltage-gated Na" channels (see p. 222). Due to their high equilibrium potential (see A), Na" ions flow into the cell and reverse the local membrane potential (depolarization). 

Figure 13.19. Membrane Potential. Depolarization of an axon membrane results in an action potential. Time course of (A) the change in membrane potential and (B) the change in Na+ and K+ conductances.

Figure 1 (a) The transmembrane topology of a hERG potassium channel subunit is depicted, (b) hERG potassium channel state is dependent on membrane potential. Depolarization favors the open (O) and inactivated (I) states, while hyperpolarization induces channel closing (C). 

Thymoquinone. Thymoquinone (TQ) is the main constituent of the oil extracted from Nigella sativa seeds, with antioxidant and anti-inflammatory effects. Treatment with TQ efficiently attenuates APi 2-induced neurotoxicity, inhibits the mitochondrial membrane potential depolarization and ROS generation caused by Api 2, restores synaptic vesicle recycling inhibition, partially reverses the loss of spontaneous firing activity, and inhibits A(f aggregation in vitro [291],... 

Schackmann, R.W., Christen, R., and Shapiro, B.M. (1981). Membrane potential depolarization and increased intracellular pH accompany the acrosome reaction of sea urchin sperm. Proc. Natl. Acad. Sci. 78 6066-6070. 

The membrane potential depolarization in pmal mutants could be explained if the mutant enzymes were less active in pumping protons across the membrane. This notion was supported by kinetic studies on ATP hydrolysis by these enzymes that showed small but significant decreases in Vmax (15). However, a dilemma arose when whole cell medium acidification experiments were performed, which reflect the action of the H+-ATPase in vivo. The rate of glucose-induced proton efflux by pmal mutant cells was found to be considerably better than that of wild-type cells (Figure 2). Only when high external K+ was included in the medium to minimize differences in membrane potential between mutant and wild-type cells did the activity of the... 

End-plate membrane potential Depolarized to -55 mV Repolarization toward -80 mV... 

Figure 13 (A) Nicotinic ACh receptor in NEB cells of neonatal hamster lung. ACh-iaduced inward current under normoxia and hypoxia conditions (p02 = 20 mmHg. Holding potential was —60 mV). (B) Application of nicotine evoked an inward current (a). Holding potential was —60 mV Effects of holding potential on inward currents evoked by 50 pM nicotine. Each plotted point is the mean peak inward current amphtude taken from between five and eight cells at each holding potential, (c) Nicotine evoked a membrane potential depolarization, (d) The peak currents evoked at each concentration are expressed relative to the peak current evoked by 50 mM nicotine and plotted against the log [nicotine] mean response taken from five to eight cells. The experimental data were fitted by the Hill equation with a Hill coefficient of 0.9 and EC50 = 4 pM.

Automa-ticity. Special cardiac cells, such as SA and AV nodal cells, His-bundle cells, and Purkinje fibers, spontaneously generate an impulse. This is the property of automaticity. Ectopic sites can act as pacemakers if the rate of phase 4 depolarization or resting membrane potential is increased, or the threshold for excitation is reduced. 

Inward Rectification refers to decreased conductance upon membrane depolarization. In classical inward rectifier K+ channels, rectification is strong and currents rapidly decline at membrane potentials positive to the reversal potential, in contrast to other Kir channels in which rectification is weak and currents decline only gradually at potentials positive to the reversal potential. 

Repolarization is a return of membrane potential to its resting value. It refers mostly to repolarization of an action potential, although a more general meaning of returning a membrane potential back to a more negative value after (forced) depolarization is also common. 

Kv-channels are closed in the resting state. Upon depolarization of the cellular membrane potential, closed Kv-channels undergo a series of voltage-dependent activating steps until they reach an activated state from which they can open and close in a voltage-independent manner. 

Figure 4. Effects of dihydro-brevetoxin B (H2BVTX-B) on Na currents in crayfish axon under voltage-clamp. (A) A family of Na currents in control solution each trace shows the current kinetics responding to a step depolarization (ranging from -90 to -I-100 mV in 10 mV increments). Incomplete inactivation at large depolarizations is normal in this preparation. (B) Na currents after internal perfusion with H2BVTX-B (1.2 a M). inactivation is slower and less complete than in the control, and the current amplitudes are reduced. (C) A plot of current amplitudes at their peak value (Ip o, o) and at steady-state (I A, A for long depolarizations) shows that toxin-mOdified channels (filled symbols) activate at more negative membrane potentials and correspond to a reduced peak Na conductance of the axon (Reproduced with permission from Ref. 31. Copyright 1984 American Society for Pharmacology and Experimental Therapeutics).

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