Neuropeptide Y Y1 receptors in the central nucleus of amygdala mediate the anxiolytic-like effect of allopregnanolone in mice: Behavioral and immunocytochemical evidences

Gajanan S. Deo, Manoj P. Dandekar, Manoj A. Upadhya, Dadasaheb M. Kokare, Nishikant K. Subhedar

Research output: Contribution to journalArticle

Abstract

Since allopregnanolone (ALLO) elicits anxiolytic-like action and increases neuropeptide Y Y1 (NPY Y1) receptors gene expression in the amygdala, we were interested in studying the involvement of NPY Y1 receptors in the anxiolytic-like actions of ALLO. The anxiety-like behavior was evaluated in mice using Vogel's conflict test (VCT), in which number of shocks were measured. ALLO and NPYergic agents, alone or in combinations, were administered bilaterally into the central nucleus of amygdala (CeA). The intra-CeA administration of ALLO, NPY or NPY Y1/Y5 receptors agonist [Leu31, Pro34]-NPY resulted in dose-dependent increase in the number of shocks in VCT, indicating anxiolytic-like effect. However, opposite effect was observed following administration of selective NPY Y1 receptors antagonist BIBP3226. While prior administration with NPY or [Leu31, Pro34]-NPY, at the subeffective dose, potentiated the ALLO-induced anxiolytic-like effect, the same was antagonized by BIBP3226. Further, the effect of acute ALLO (30 mg/kg, intraperitoneal) on the endogenous NPY system in the CeA, ventral part of lateral division of bed nucleus of the stria terminalis (BSTLV), nucleus accumbens core (AcbC) and arcuate nucleus (ARC) was studied with immunocytochemistry. Acute ALLO treatment significantly decreased the population of NPY-immunoreactive cells in the CeA and also in the ARC. While NPY-immunoreactive fibers were slightly increased in the AcbC and BSTLV, the cells in AcbC and fibers in ARC did not respond. We suggest that NPY may mediate ALLO induced anxiolytic-like behavior in the neuroanatomical framework of the CeA, possibly via NPY Y1 receptors.
Original languageEnglish
Pages (from-to)77-86
JournalBrain Research
Volume1318
DOIs
Publication statusPublished - 8 Mar 2010

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