Opioid receptor subtype antagonists differentially alter GABA agonist-induced feeding elicited from either the nucleus accumbens shell or ventral tegmental area regions in rats

Food intake is significantly increased by administration of either GABA _A (e.g., muscimol) or GABA _B (e.g., baclofen) agonists into either the shell region of the nucleus accumbens (NAC) or the ventral tegmental area (VTA); these responses are selectively blocked by pretreatment with corresponding GABA _A and GABA _B antagonists. Previous studies found that a single dose (5 μg) of the general opioid antagonist, naltrexone reduced feeding elicited by muscimol, but not baclofen in the NAC shell, and reduced feeding elicited by baclofen, but not muscimol in the VTA. The present study compared feeding responses elicited by either muscimol or baclofen in either the VTA and NAC shell following pretreatment with equimolar doses of selective μ (0.4, 4 μg), δ (0.4, 4 μg), or κ (0.6, 6 μg) opioid receptor subtype antagonists. Muscimol (25 ng) and baclofen (200 μg) each significantly and equi-effectively increased food intake over 4 h following VTA or NAC shell microinjections. Muscimol-induced feeding elicited from the VTA was significantly enhanced by μ or δ antagonists, and was significantly reduced by κ antagonists. Baclofen-induced feeding elicited from the VTA was significantly reduced by μ or κ, but not δ antagonists. Muscimol-induced feeding elicited from the NAC was significantly reduced by either μ, κ or δ antagonists. Baclofen-induced feeding elicited from the NAC was significantly reduced by κ or δ, but not μ antagonists. These data indicate differential opioid receptor subtype antagonist-induced mediation of GABA receptor subtype agonist-induced feeding elicited from the VTA and NAC shell. This is consistent with previously demonstrated differential GABA receptor subtype antagonist-induced mediation of opioid-induced feeding elicited from these same sites. Thus, functional relationships exist for the elaborate anatomical and physiological interactions between these two neurochemical systems in the VTA and NAC shell.