Effects of Nitric Oxide on Protein—Lipid Interactions in the Membranes of the Myelinated Nerve Fiber

摘要

The influence of nitric oxide (NO) on the myelinated nerve fiber and the impact of modification of SH-groups of axon and myelin membrane proteins on the amplitude and propagation velocity of action potential (AP),amount of the membrane-bound calcium (Ca_(mb)~(2+)),viscosity of the axon membrane, and saturation factor of phos-pholipid fatty acids (SO of myelin have been investigated. We established that the decrease in the number of extra-cellular SH-groups in membrane proteins induced by p-chloromercuribenzoate (pCMB, 10~(-4)M), led to a decrease in the AP amplitude and a reversible desorption of C a_(mb)~(2+)but did not affect the axolemma viscosity and Sf. Nitricoxide (NO) caused a decrease in the AP amplitude and propagation velocity, an increase in the axolemma viscosityand a decrease in Sf of myelin; it also induced a reversible desorption of Ca_(mb)~(2+),. Pretreatment of the nerve fiber with pCMB weakened the NO-induced desorption of Ca_(mb)~(2+).Pretreatment of the nerve fiber with K~+-channelblocker tetraethylammonium (10~(-2)M) completely abolished the NO-induced change in amount of Ca_(mb)~(2+). Wesuppose that NO-mediated changes in axolemma viscosity, Sf of myelin and desorption of Ca_(mb)~(2+)affect protein-lipid interactions in axolemma and myelin, which in their turn influence the propagation of AP.