Nerve cell resting potential

Other ion channels are closed at rest, but may be opened by a change in membrane potential, by intracellular messengers such as Ca + ions, or by neurotransmitters. These are responsible for the active signalling properties of nerve cells and are discussed below (see Hille 1992, for a comprehensive account). A large number of ion channels have now been cloned. This chapter concerns function, rather than structure, and hence does not systematically follow the structural classification. 

The electricity-producing system of electric fishes is built as follows. A large number of flat cells (about 0.1 mm thick) are stacked like the flat unit cells connected in series in a battery. Each cell has two membranes facing each other. The membrane potentials of the two membranes compensate for each other. In a state of rest, no electrostatic potential difference can be noticed between the two sides of any cell or, consequently, between the ends of the stack. The ends of nerve cells come up to one of the membranes of each cell. When a nervous impulse is applied from outside, this membrane is excited, its membrane potential changes, and its permeability for ions also changes. Thus, the electrical symmetry of the cell is perturbed and a potential difference of about 0.1 V develops between the two sides. Since nervous impulses are applied simultaneously to one of the membranes in each cell, these small potential differences add up, and an appreciable voltage arises between the ends of the stack. 

Table 3.1 Concentration and Permeability of Ions Responsible for Membrane Potential in a Resting Nerve Cell...

This results in the extrusion of three positive charges for every two that enter the cell, resulting in a transmembrane potential of 50-70 mV, and has enormous physiological significance. More than one-third of the ATP utilized by resting mammalian cells is used to maintain the intracellular Na+-K+ gradient (in nerve cells this can rise up to 70%), which controls cell volume, allows neurons and muscle cells to be electrically excitable, and also drives the active transport of sugars and amino acids (see later). 

The initiation of an epileptic attack involves "pacemaker" cells these differ from other nerve cells in their unstable resting membrane potential, i.e a depolarizing membrane current persists after the action potential terminates. 

The two processes briefly lead to the charge even falling below the resting potential (hyperpolarization). The channels also close after a few milliseconds. The nerve cell is then ready for re-stimulation. 

In a resting condition, there is a specific rest potential between the axoplasm and the inner parts of the cell. This rest potential is maintained by relative concentration of sodium and potassium ions along the membrane of the nerve. During nerve stimulation, the membrane is depolarized and sodium channels in that area are opened, allowing sodium ions to rush into the cell. At the peak of depolarization potassium channels are opened. The last ones leave the cell and the cell is repolarized. 

Action potentials are waves of depolarization and repolarization of the plasma membrane. In a resting nerve cell, the electric potential gradient (At//) across the plasma membrane is about —70 mV, inside negative. This potential difference is generated mainly by the unequal rates of diffusion of K+ and Na+ ions down concentration gradients maintained by the Na+-K+ ATPase. 

We may extrapolate from these basic considerations in two ways. We may evaluate the extracellular electric gradients associated with intrinsic or imposed tissue fields against the magnitude of the gradients in the membrane potential, both in resting conditions and in association with modification of the membrane potential during synaptic excitation. In this way, we may appraise the probability of direct effects of extracellular tissue fields in excitation of nerve cells. A second approach will consider the observed biological sensitivities to these fields. This will lead to the crux of our current dilemma. A... 

Bioelectric Organization of Nervous Tissue. The membrane potential of 70 mV is developed across the lipid bilayer of the cell membrane. This layer is approximately 40 8 thick, so that the transmembrane electric gradient is of the order of 105 V/cm. This extraordinary dielectric strength is not easily replicated in artificial materials. It is noteworthy that the resting membrane potential maintains this dielectric bilayer within a factor of two of electrical breakdown (19). Release of neural transmitter substances from synaptic terminals on the nerve cell surface transiently shifts the membrane potential at the site of release by a few millivolts. In terms of an altered transmembrane gradient, this shift is of the order of 1.0 kV/cm. 

This statement requires explanation in terms of the electrical double layer at the surface of all cells, including at the sarcolemma of myofibers and the plasma membrane of neurons. The inner part of this double layer (Stmt layer) can be regarded as a condenser with its complement of ions largely giving it a certain numerical value for permittivity (dielectric constant). This is charged when the membranes of muscle and nerve are at rest (resting potential). 

The normal potential difference between the inner and outer parts of nerve cells is about -70 mv as estimated above. Transmission of a nerve impulse is initiated by a lowering of this potential difference to about -20 mv. This has the effect of temporarily opening the Na+ channel the influx of these ions causes the membrane potential of the adjacent portion of the nerve to collapse, leading to an effect that is transmitted along the length of the nerve. As this pulse passes, K+ and Na+ pumps restore the nerve to its resting condition. 

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