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 alpha-methyl-p-tyrosine. On the whole, Mg(2+)-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.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Viola MS,Rodríguez de Lores Arnaiz G,Enero MAdoi
10.1016/0197-0186(94)90133-3subject
Has Abstractpub_date
1994-01-01 00:00:00pages
91-7issue
1eissn
0197-0186issn
1872-9754journal_volume
24pub_type
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