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  2. Medial amygdaloid nucleus 5-HT₂c receptors are involved in the hypophagic effect caused by zimelidine in rats

Medial amygdaloid nucleus 5-HT₂c receptors are involved in the hypophagic effect caused by zimelidine in rats

  • Neuropharmacology. 2012 Aug;63(2):301-9. doi: 10.1016/j.neuropharm.2012.03.020.
A A Scopinho 1 E A T Fortaleza F M A Corrêa L B M Resstel
Affiliations

Affiliation

  • 1 Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Bandeirantes Avenue 3900, 14049-900 Ribeirão Preto, SP, Brazil. [email protected]
Abstract

The medial amygdaloid nucleus (MeA) is a sub-region of the amygdaloid complex that has been described as participating in food intake regulation. Serotonin has been known to play an important role in appetite and food intake regulation. Moreover, serotonin 5-HT(2C) and 5-HT(1A) receptors appear to be critical in food intake regulation. We investigated the role of the serotoninergic system in the MeA on feeding behavior regulation in rats. The current study examined the effects on feeding behavior regulation of the serotonin reuptake inhibitor, zimelidine, administered directly into the MeA or given systemically, and the serotoninergic receptors mediating its effect. Our results showed that microinjection of zimelidine (0.2, 2 and 20 nmol/100 nL) into the MeA evoked dose dependent hypophagic effects in fasted rats. The selective 5-HT(1A) receptor antagonist WAY-100635 (18.5 nmol/100 nL) or the 5-HT(1B) receptor antagonist SB-216641 microinjected bilaterally into the MeA did not change the hypophagic effect evoked by local MeA zimelidine treatment. However, microinjection of the selective 5-HT(2C) receptor antagonist SB-242084 (10 nmol/100 nL) was able to block the hypophagic effect of zimelidine. Moreover, microinjection of the 5-HT(2C) receptor antagonist SB-242084 into the MeA also blocked the hypophagic effect caused by zimelidine administered systemically. These results suggest that MeA 5-HT(2C) receptors modulate the hypophagic effect caused by local MeA administration as well as by systemic zimelidine administration. Furthermore, 5-HT(2C) into the MeA could be a potential target for systemic administration of zimelidine.

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