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Desipramine modulates 3H-ouabain binding in rat hypothalamus
M S Viola1, M C Antonelli, M A Enero
1Instituto de Biología Celular y Neurociencias, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Journal of Neuroscience Research
|January 1, 1997
Summary
Acute desipramine (DMI) treatment increases Na+, K+-ATPase activity and ouabain binding sites in the rat hypothalamus, suggesting indirect stimulation via noradrenaline.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Previous studies demonstrated increased hypothalamic Na+, K+-ATPase activity after acute desipramine (DMI) administration.
- Desipramine is a selective noradrenaline (norepinephrine) reuptake inhibitor.
Purpose of the Study:
- To investigate the effect of acute DMI treatment on ouabain binding sites and Na+, K+-ATPase activity in rat brain.
- To explore the mechanism of DMI's action on Na+, K+-ATPase in specific brain regions.
Main Methods:
- Quantitative autoradiography was used to measure 3H-ouabain binding in rat brain sections.
- Potassium-stimulated p-nitrophenylphosphatase activity was assessed in hypothalamic and cerebral cortex membranes.
Main Results:
- Acute DMI administration (10 mg/kg) significantly increased the number of ouabain binding sites in the hypothalamus, but not the cerebral cortex.
- Concomitant enhancement of K+-stimulated p-nitrophenylphosphatase activity was observed in hypothalamic membranes, with no change in cerebral cortex membranes.
- In vitro studies confirmed that DMI directly inhibits Na+, K+-ATPase, ruling out direct interaction.
Conclusions:
- Acute DMI treatment indirectly stimulates hypothalamic Na+, K+-ATPase, likely mediated by increased noradrenaline levels.
- The observed changes are specific to the hypothalamus and not the cerebral cortex.
- Noradrenaline may act on the external phosphorylated site of the Na+, K+-ATPase to mediate this indirect stimulation.