Cell membranes excitation

In the electric organ of fishes, a number of such stacks are connected in parallel and in series. The total voltage attains 500 V in the electric eel. A current pulse of about 0.5 A develops when this voltage appears across an external circuit (in fresh water or seawater). For the electric ray, these numbers are 60 V and 50 A, respectively. The length of such an electric pulse is comparable with the time of cell membrane excitation (i.e., 1 to 2ms, which is quite sufficient to defeat a designated victim). Some species of fish use pulses repeated at certain intervals. 

Hypocalcemia occurring with calcium chelators, magnesium antagonism, or certain loop diuretics may produce muscle spasm and tetanic contractions in most species by increasing cell membrane excitability of motor neurons with resultant increased neuromuscular transmission. Interestingly, flaccid paralysis and recumbency in... 

Loss of cell membrane excitability causes cardiac symptoms. 

Ion Channels. The excitable cell maintains an asymmetric distribution across both the plasma membrane, defining the extracellular and intracellular environments, as well as the intracellular membranes which define the cellular organelles. This maintained a symmetric distribution of ions serves two principal objectives. It contributes to the generation and maintenance of a potential gradient and the subsequent generation of electrical currents following appropriate stimulation. Moreover, it permits the ions themselves to serve as cellular messengers to link membrane excitation and cellular... 

Maintenance of electrical potential between the cell membrane exterior and interior is a necessity for the proper functioning of excitable neuronal and muscle cells. Chemical compounds can disturb ion fluxes that are essential for the maintenance of the membrane potentials. Fluxes of ions into the cells or out of the cells can be blocked by ion channel blockers (for example, some marine tox-... 

Potassium channels are a diverse and ubiquitous family of membrane proteins present in both excitable and nonexcitable cells that selectively conduct K+ ions across the cell membrane along its electrochemical gradient at a rate of 106-108 ions/s. 

TRPM4 also known as the Ca2+-activated nonselective cation (CAN-) channel, mediates cell membrane depolarization in many excitable and nonexcitable cells. 

Figure 3. Reporting of intracellular calcium sequestration by chlorotetracycline (CTC). CTC preferentially partitions into cell membranes and its fluorescence in this environment is sensitive to calcium bound to the membrane therefore its signal (excitation AOO nm, emission 530 nm) will come largely from organelles that bind or sequester calcium, such as smooth endoplasmic reticulum or mitochondria. Release of calcium from such organelles is accompanied by dissociation of the calcium-CTC complex, a decrease in CTC fluorescence and efflux of unbound probe from the organelle and from the cell.

In many epithelia Cl is transported transcellularly. Cl is taken up by secondary or tertiary active processes such as Na 2Cl K -cotransport, Na Cl -cotransport, HCOJ-Cl -exchange and other systems across one cell membrane and leaves the epithelial cell across the other membrane via Cl -channels. The driving force for Cl -exit is provided by the Cl -uptake mechanism. The Cl -activity, unlike that in excitable cells, is clearly above the Nernst potential [15,16], and the driving force for Cl -exit amounts to some 2(f-40mV. 

FIGURE 30.3 Changes in membrane potential cp of a cell membrane occurring upon application of depolarizing current pulses of different amplitude / (a,b) below threshold (c) excitation of the membrane during an above-threshold pulse. 

Prize in Medicine for their work on the excitation of cell membranes and of nerve impnlse propagation. 

While many biological molecules may be targets for oxidant stress and free radicals, it is clear that the cell membrane and its associated proteins may be particularly vulnerable. The ability of the cell to control its intracellular ionic environment as well as its ability to maintain a polarized membrane potential and electrical excitability depends on the activity of ion-translocating proteins such as channels, pumps and exchangers. Either direct or indirect disturbances of the activity of these ion translocators must ultimately underlie reperfiision and oxidant stress-induced arrhythmias in the heart. A number of studies have therefore investigated the effects of free radicals and oxidant stress on cellular electrophysiology and the activity of key membrane-bound ion translocating proteins. 

Mueller, P. Rudin, D. O. Tien, H. T. Westcott, W. C., Reconstitution of cell membrane structure in vitro and its transformation into an excitable system, Nature 194, 979-980 (1962). 

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