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- W2023453237 abstract "ATPase activities in CNS membranes were studied after administration of desipramine (DMI), a noradrenaline (NA) uptake inhibitor. In a previous paper we reported that Na+, K+-ATPase activity significantly increased 3 h after DMI administration (10 mg/kg) in hypothalamus and mesencephalus but not in cerebral cortex and pons-medulla oblongata membranes (Viola et al., Cell. molec. Neurobiol. 1989, 9, 263–271). Here it was observed that Na+, K+-ATPase increase induced by acute DMI disappeared at 24 h in hypothalamus but remained during 21 days in mesencephalus. Na+, K+-ATPase increase by acute DMI was inhibited when endogenous NA was depleted by the noradrenergic neurotoxin DSP-4 or the NA synthesis inhibitor α-methyl-p-tyrosine. On the whole, Mg2+-ATPase activity was not modified by treatment. 5′-nucleotidase, another membrane-bound enzyme, was unchanged by acute DMI. The addition of DMI in vitro (50 ng/mg tissue) during Na+, K+-ATPase assay failed to affect ATPase activities. Acute DMI effects on Na+, K+-ATPase are thus attributable to noradrenergic neurotransmission rather than to non-specific drug-CNS membrane interaction. Furthermore, DMI produces differential effects on membrane Na+, K+-ATPase, depending on treatment conditions and CNS area studied." @default.
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- W2023453237 title "Na+, K+-ATPase activity in CNS and noradrenergic neurotransmission: time course of differential desipramine (DMI) effects" @default.
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- W2023453237 doi "https://doi.org/10.1016/0197-0186(94)90133-3" @default.
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