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Desipramine modulates 3 H‐ouabain binding in rat hypothalamus
Author(s) -
Viola M.S.,
Antonelli M.C.,
Enero M.A.,
Rodríguez de Lores Arnaiz G.
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19970101)47:1<77::aid-jnr8>3.0.co;2-c
Subject(s) - desipramine , ouabain , hypothalamus , endocrinology , medicine , cerebral cortex , chemistry , cortex (anatomy) , enzyme , atpase , biology , hippocampus , biochemistry , neuroscience , sodium , organic chemistry , antidepressant
We have previously shown that Na + , K + ‐ATPase activity in hypothalamus is increased after administration of an acute dose of desipramine, a noradrenaline uptake inhibitor (Viola et al., Cell Molec Neurobiol 9:263–271, 1989). In this report the same treatment (10 mg per kg) was applied to evaluate 3 H‐ouabain binding in rat brain sections by quantitative autoradiography. Results disclosed an increase in the number of ouabain binding sites in hypothalamus but not in cerebral cortex. Concomitantly, such acute DMI treatment enhanced K + ‐stimulated‐ p ‐nitrophenylphosphatase activity in hypothalamus membranes whereas it failed to modify cerebral cortex membranes. A direct interaction of DMI with the enzyme was ruled out since in vitro DMI is known to inhibit the enzyme. It may be speculated that DMI indirectly stimulates Na + , K + ‐ATPase through the increase in noradrenaline which acts in turn on the external phosphorylated site of the enzyme. J. Neurosci. Res 47:77–82, 1997. © 1997 Wiley‐Liss, Inc.