Effects of nitric oxide on protein-lipid interactions in the membranes of the myelinated nerve fiber

The influence of nitric oxide (NO) on the myelinated nerve fiber and the impact of modification of SHgroups 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 phospholipid fatty acids (Sf) of myelin have been investigated. We established that the decrease in the number of extracellular 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 Ca mb 2+ but did not affect the axolemma viscosity and Sf. Nitric oxide (NO) caused a decrease in the AP amplitude and propagation velocity, an increase in the axolemma viscosity and 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 Pretreatment of the nerve fiber with K+-channel blocker tetraethylammonium (10−2 M) completely abolished the NO-induced change in the amount of Ca mb 2+ . We suppose 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.