Evoked ventromedial hypothalamic activity: Changes produced by drugs which modify female sexual behavior in the rat

The effect of several pharmacologic agents on the field potential and multiunit responses evoked in the ventromedial hypothalamic nucleus (VMN) by single shocks applied to the anterior part of the amygdaloid nucleus and the posterior part of the lateral amygdaloid nucleus was investigated in ovariec...

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Veröffentlicht in:Experimental neurology 1983-01, Vol.82 (2), p.270-286
Hauptverfasser: Mascó, Daniel H., Carrer, Hugo F.
Format: Artikel
Sprache:eng
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Zusammenfassung:The effect of several pharmacologic agents on the field potential and multiunit responses evoked in the ventromedial hypothalamic nucleus (VMN) by single shocks applied to the anterior part of the amygdaloid nucleus and the posterior part of the lateral amygdaloid nucleus was investigated in ovariectomized (OVX) and proestrous (PRO) rats using a combined infusion cannula and recording electrode. The local infusion of carbamylcholine and eserine incremented the multiunitary responses, whereas atropine, hexamethonium, and hemicholinium suppressed the multiunit responses and, in the case of atropine, the field response also. The onset of the suppressive effect of hemicholinium depended on the activation of the amygdaloid input. Phenoxybenzamine, methysergide, and picrotoxin increased the multiunitary evoked responses in OVX, but phenoxybenzamine and methysergide had no effect on PRO rats. On the contrary, propanolol suppressed the response. Because a good correlation can be observed between the effects of drugs on evoked responses and on sexual behavioral responses (lordosis) of the female rat as reported in the literature, the results are compatible with the hypothesis that (a) amygdaloid influences on sexual behavior are exerted through modifications of neuron activity in the VMN, (b) this influence involves the activation of a cholinergic synapse, and (c) catecholaminergic, GABAergic, and serotoninergic inputs modulate VMN neuron responses to activity originated in the amygdala.
ISSN:0014-4886
1090-2430
DOI:10.1016/0014-4886(83)90401-6