Nerve membrane perturbation

The mean slope for the 17 examples of Table II is 1.07 . 14. The equations have been ordered with respect to intercept with an overall difference in this parameter of about 1 log unit. Thus, narcosis of tadpoles requires about one-tenth lower concentration of drug than the 50% inhibition of indophenol oxidase (Equation 3). The equation most nearly resembling the model equation (Equation 18) is Equation 6 correlating the structure-activity relationship between the concentration of ROH necessary to produce a 5-mv change in the rest potential of the lobster axon. This close relationship between hemolysis and nerve membrane perturbation has been noted by others using different techniques (II, 12). The relationships of Table II show that different sets of molecules acting on very different systems can be compared quickly in numerical terms. 

The testing of pure optical isomers can give much insight into the nature of a receptor. An example concerns the anaesthetic gases. It is widely believed that anaesthetic gases exert their action by a structurally nonspecific perturbation of the fluid character of nerve membranes. This view... 

FIGURE 11-2 Schematic illustration of two possible ways general anesthetics may act on the nerve membrane. In the general perturbation theory, anesthetic molecules lodge in the lipid bilayer and inhibit sodium channel function by disrupting membrane structure. In the specific receptor theory, anesthetics inhibit the opening of the sodium channel by binding directly to the channel protein. 

This question of direct interaction with nerve proteins or indirect interaction via membrane perturbation has also been tackled by ESR spectroscopy. Two types of labeling have been used fatty acids for lipid labeling and maleimide for frog nerve proteins. The anesthetics used were halothane as an example of a general anesthetic and procaine, lidocaine, and tetracaine as examples of local anesthetics. The latter interact primarily with head groups but can also merge into the hydrophobic hydrocarbon... 

A model, based on a perturbation analysis of the highly successful empirical formulation of Hodgkin and Huxley (1), has been developed which makes predictions of the effect of oscillating fields on a particular nerve membrane system (2). In the present paper, a theoretical model will be presented along with some of the predicted effects of AC electric fields on the Hodgkin-Huxley (HH) model of squid axon membranes. 

Section (4) refers to the restrictions imposed on cation movement by membranes. The relative ease of movement of potassium through a nerve membrane at rest generates a potassium potential. Imposition of a perturbation upon the membrane changes its properties so that it is more permeable to sodium, and the activated membrane shows a sodium potential of reversed sign to the potassium potential. Thereupon a self-propagating spike of depolarization which is rapidly followed by recovery to the rest state fiows along the nerve cell and is the nerve message. 

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. 

These equations offer an adequate basis for the development of the negative membrane potential of 70 to 90 mV. Excitation as a process characterizing nerve and muscle cells is associated with a transient reduction or abolition of this membrane potential, and in some cases with a temporary "overshoot" or reversal of its polarity. Just as for the membrane potential, these major but transient perturbations in the production of action potentials have been adequately modeled in dynamics of ionic equilibria by Hodgkin and Huxley (2). 

There are additional changes in diabetic nerve of experimental animals that will not be considered in detail here. These include, but are not limited to, diminished Na, K -ATPase activity, which can have adverse effects on the maintenance of the nerve resting membrane potential and perturbation of neurotrophic support. All of these pathological processes, acting in concert, lead not only to decreased nerve conduction velocity but also to reduced nerve blood flow, a condition beUeved to induce endoneurial hypoxia. Over the... 

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