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Norepinephrine‐Stimulated Increase in Na + ,K + ‐ATPaseActivity in the Rat Brain Is Mediated Throughα 1A ‐Adrenoceptor Possibly by Dephosphorylation of the Enzyme
Author(s) -
Mallick Birendra Nath,
Adya H. V. Anupama,
Faisal Mohammad
Publication year - 2000
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 - 10.1046/j.1471-4159.2000.0741574.x
Subject(s) - prazosin , endocrinology , medicine , calmodulin , forskolin , norepinephrine , calcineurin , calcium , chemistry , adrenergic receptor , enzyme , intracellular , phosphatase , receptor , biology , biochemistry , antagonist , dopamine , transplantation
Rapid eye movement sleep deprivation is reported toincrease Na + ,K + ‐ATPase activity. This increase was shownearlier to be stimulated by norepinephrine acting onα 1 ‐adrenoceptor. The involvement of a subtype ofα 1 ‐adrenoceptor and the possible molecular mechanism ofaction of norepinephrine in increasing the enzyme activity were investigatedusing receptor agonists and antagonists, as well as stimulants and blockers ofsignal transduction pathway. It was observed that incubation of the homogenatewith cyclic AMP, forskolin, A23187 (a calcium ionophore), or calmodulin alonedid not stimulate the Na + ,K + ‐ATPase activity. However,although the spontaneous activity of the Na + ,K + ‐ATPasewas not affected by prazosin, WB4101, heparin, W13, or cyclosporin A alone,each of them could prevent the norepinephrine‐stimulated increase in theenzyme activity. Based on these results and our previous findings, it isproposed that norepinephrine acted on α 1A ‐adrenoceptor andincreased intracellular calcium, which in the presence of calmodulin activateda calmodulin‐dependent phosphatase, calcineurin. This calcineurin possiblydephosphorylated Na + ,K + ‐ATPase and increased its activity. The physiological significance especially in relation to rapid eye movement sleep deprivation is discussed.