Norepinephrine‐Stimulated Increase in Na+,K+‐ATPaseActivity in the Rat Brain Is Mediated Throughα1A‐Adrenoceptor Possibly by Dephosphorylation of the Enzyme

• DOI: 10.1046/j.1471-4159.2000.0741574.x
• Publication Date: 2003-03-12T06:44:22Z
• Authors: Birendra Nath Mal...; H. V. Anupama Adya; Mohammad Faisal
• Keywords: Male; Ionophores; Heparin; Calcineurin; Colforsin; Anticoagulants; Brain; Prazosin; Dioxanes; Enzyme Activation; Norepinephrine; 03 medical and health sciences; 0302 clinical medicine; Calmodulin; Cyclosporine; Animals; Calcium; Enzyme Inhibitors; Phosphorylation; Adrenergic alpha-Agonists; Adrenergic alpha-Antagonists; Calcimycin

Abstract: Rapid eye movement sleep deprivation is reported to increase Na + ,K ‐ATPase activity. This was shown earlier be stimulated by norepinephrine acting on α 1 ‐adrenoceptor. The involvement of a subtype ‐adrenoceptor and the possible molecular mechanism action in increasing enzyme activity were investigated using receptor agonists antagonists, as well stimulants blockers signal transduction pathway. It observed that incubation homogenate with cyclic AMP, forskolin, A23187 (a calcium ionophore), or calmodulin alone did not stimulate However, although spontaneous affected prazosin, WB4101, heparin, W13, cyclosporin A alone, each them could prevent norepinephrine‐stimulated Based these results our previous findings, it proposed acted 1A increased intracellular calcium, which presence activated calmodulin‐dependent phosphatase, calcineurin. calcineurin possibly dephosphorylated its physiological significance especially relation rapid discussed.