[The role of membrane protein SH-groups in regulating ouabain and bungarotoxin binding in the crab nerve].

Structural alterations in plasma membrane proteins promoting transition from inactive forms of Na-pump and acetylcholine receptor to active ones during propagation of rhythmic excitation were examined. The role of SH-groups of the nerve (fibre and glial cell) plasma membrane proteins in providing regulation of the pump and receptor state by generalized alterations in the membrane structure is discussed.

[The role of the state of protein-lipid interactions in stimulated membranes in the conformation of C40-carotenoids].

It was shown by Raman spectroscopy that conformation of carotenoid in the frog nerve membranes at rest and at propagation of rhythmic excitation depends on the state of protein-lipid interaction modified by exposition of the nerve in solution with trypsin, alpha-chymotrypsin, urea, glutaraldehyde, SH-reagents, isopropanol and system "Fe-ascorbate". It is suggested that the level of the protein-lipid interactions in excitable membranes with the intramembrane potential determines C40-carotenoid conformation at the propagation of rhythmic excitation by he nerve.

[Binding of 3H-bungarotoxin by nerve trunks of the frog during excitatory conduction].

In the frog nerve, 3H-bungarotoxin and 3H-acetylcholine binding increased whereas the acetylcholinesterase activity decreased in rhythmic stimulation. The enhancement of 3H-bungarotoxin binding to nerve during the rhythmic stimulation seems to stem from transformation of "inactive" forms of acetylcholine receptor of glial membrane to "active" ones.

[Changes in the permeability of nerve fiber membranes during the initiation of lipid peroxidation].

The role of lipid oxidation in the mechanism of ion transport was investigated. During initiation of lipid oxidation by actin "Fe2+--ascorbic acid" in the crab nerve 45Ca and 22Na accumulation and level of lipid oxidation were increased, but electric stimulation of the nerve greatly changed ion accumulation. Increased Na+Ca2+ accumulation during the initiation of lipid oxidation is explained not only by changes in the lipid phase of excitable membranes but by the effects of rhythmic excitation on potential-dependent channels.