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Brain Na + , K + ‐ATPase: Alteration of Ligand Affinities and Conformation by Chronic Ethanol and Noradrenergic Stimulation In Vivo
Author(s) -
Swann Alan C.
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb00669.x
Subject(s) - yohimbine , chemistry , stimulation , ethanol , in vivo , norepinephrine , medicine , endocrinology , atpase , ligand (biochemistry) , biophysics , biochemistry , receptor , enzyme , biology , antagonist , dopamine , microbiology and biotechnology
These experiments examined effects of chronic ethanol, repeated noradrenergic stimulation or inhibition, and ethanol combined with the noradrenergic treatments on regulation of Na + , K + ‐ATPase. Chronic treatment with ethanol reduced the sensitivity of K + ‐ p ‐nitrophenyl‐phosphatase to ethanol, increased affinity for K + , reduced the sensitivity of K + affinity to ATP or ethanol, and reduced Δ H and Δ S for K + activation and for the E1–E2 transition. These effects were all opposite to those of ethanol added in vitro. Treatment with yohimbine had the opposite effects on ethanol sensitivity, K + affinity, K + interactions with ethanol and ATP, and thermodynamic parameters for cation activation or conformational change. These effects were similar to those of norepinephrine in vitro. The effects of yohimbine treatment were eliminated or reduced in rats also treated with ethanol. Depletion of norepinephrine had effects opposite to those of yohimbine. These data are consistent with a reduction in membrane fluidity, at least in the vicinity of Na + , K + ‐ATPase, during ethanol tolerance. Exposure to norepinephrine, in vitro or in vivo, had effects on Na + , K + ‐ATPase that were similar to those of increased membrane fluidity. Key Words: Na + , K + ‐ATPase—Ethanol—Norepinephrine—Membrane effects—Ethanol tolerance—Yohimbine. Swann A. C. Brain Na + , K + ‐ATPase: Alteration of ligand affinities and conformation by chronic ethanol and noradrenergic stimulation in vivo. J. Neurochem . 47, 707–714 (1986).