Potassium channels membrane potential

Figure 6. Resting membrane potential under normoxia (left) and ischemia (right). Increased outward potassium current during ischemia causes shortening of the resting membrane potential. Potassium currents activated under physiological conditions are inhibited under ischemia and several other new channels come to the operation (IKATp, IKFFA). Resting membrane potential is less negative due to the increased extracellular potassium and inward currents.

Biological Applications Measuring membrane potential HCN channel modulators potassium channel openers"... 

The resting membrane potential of most excitable cells is around —60 to —80 mV. This gradient is maintained by the activity of various ion channels. When the potassium channels of the cell open, potassium efflux occurs and hyperpolari2ation results. This decreases calcium channel openings, which ia turn preveats the influx of calcium iato the cell lea ding to a decrease ia iatraceUular calcium ia the smooth muscles of the vasculature. The vascular smooth muscles thea relax and the systemic blood pressure faUs. 

CFTR has a single-channel conductance of about 8 pS. It is present in the apical membranes of many epithelia. Its mutation leads to the potentially lethal disease cystic fibrosis. In addition to acting as a chloride channel, CFTR is also thought to regulate, e.g., the epithelial sodium channel ENaC, a molecularly unknown outwardly-rectifying chloride channel, and possibly also potassium channels and water channels. Some of these potential regulatory processes, however, are controversial. CFTR also acts as a receptor for bacteria. 

Voltage-gated potassium (Kv) channels are membrane-inserted protein complexes, which form potassium-selective pores that are gated by changes in the potential across the membrane. The potassium current flow through the open channel follows by the electrochemical gradient as defined by the Nernst equation. In general, Kv channels are localized in the plasma membrane. 

Ordinarily, when the current pulse is over, the excess charges will be drained through the passive transport channels, and by operation of the sodium-potassium pumps the original values of membrane potential and of the concentration gradients will be reestablished. However, when in the case of depolarization the negative value of cp has dropped below a certain threshold value, which is about -50 mV, the picture changes drastically Excitation of the membrane occurs. When the current is turned off, the membrane potential not only fails to be restored but continues to... 

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... 

Fig. 6.20 Time dependence of the membrane current. Since the potassium channel is blocked the current corresponds to sodium transport. The upper line represents the time course of the imposed potential difference. (According to W. Ulbricht)...

Fig. 6.21 Joint application of patch-clamp and voltage-clamp methods to the study of a single potassium channel present in the membrane of a spinal-cord neuron cultivated in the tissue culture. The values indicated before each curve are potential differences imposed on the membrane. The ion channel is either closed (C) or open (O). (A simplified drawing according to B. Hille)...

Fig. 6.24 A hypothetic scheme of the time behaviour of the spike linked to the opening and closing of sodium and potassium channels. After longer time intervals a temporary hyperpolarization of the membrane is induced by reversed transport of potassium ions inside the nerve cell. Nernst potentials for Na+ and K+ are also indicated in the figure. 

Several different changes in mitochondria occur during apoptosis. These include a change in membrane potential (usually depolarization), increased production of reactive oxygen species, potassium channel activation, calcium ion uptake, increased membrane permeability and release of cytochrome c and apoptosis inducing factor (AIF) [25]. Increased permeability of the mitochondrial membranes is a pivotal event in apoptosis and appears to result from the formation of pores in the membrane the proteins that form such permeability transition pores (PTP) may include a voltage-dependent anion channel (VDAC), the adenine nucleotide translocator, cyclophilin D, the peripheral benzodiazepine receptor, hexokinase and... 

Valproic acid may potentiate postsynaptic GABA responses, may have a direct membrane-stabilizing effect, and may affect potassium channels. 

In sum, the natural tendency will be for sodium, calcium, and chloride ions to flow into the neuron and for potassium ions to flow out, and in so doing to reduce the membrane potential to zero. In reality, this is not so easy. The plasma membrane of the neuron is not very permeable to these ions. If it were, it would be impossible to sustain concentration gradients across it. The rate of passive diffusion of these ions across this membrane is very slow, though not zero, and different for each ion. So how do ions get across the neuronal plasma membrane rapidly There are two ways gated channels and active transport by pumps. 

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