Muscarinic, nicotinic and GABAergic receptor signaling differentially mediate fat-conditioned flavor preferences in rats.

Rats display conditioned flavor preferences (CFP) for fats. Previous studies demonstrated that whereas expression of an already-acquired corn oil (CO)-CFP was mildly reduced by dopamine (DA) D1, DA D2, NMDA or opioid receptor antagonists, the acquisition or learning of CO-CFP was eliminated by NMDA antagonists, and significantly reduced by DA D1 and D2, but not opioid antagonists. Previous studies of fructose-CFP demonstrated that muscarinic (scopolamine) and nicotinic (mecamylamine) cholinergic receptor antagonists and GABA (baclofen) receptor agonism reduced the expression of this acquired response, and that scopolamine, but not mecamylamine or baclofen eliminated the acquisition or learning of this response. The present study examined scopolamine, mecamylamine or baclofen effects upon expression or acquisition of CO-CFP. For expression, rats were trained over 10 sessions with CS+ (3.5% CO) and CS- (0.9% CO) flavored solutions without drugs. Two-bottle choice tests with CS+ and CS- flavors in 0.9% CO examined preferences following vehicle, scopolamine (1-10mg/kg), mecamylamine (1-8mg/kg) and baclofen (1.5-5mg/kg). In acquisition, eight groups of rats received vehicle, scopolamine (1, 2.5mg/kg), mecamylamine (4, 6mg/kg), baclofen (3, 5mg/kg) or a limited intake vehicle control 0.5h prior to all 10 CS+ and CS- training sessions followed by six 2-bottle CS+ and CS- choice tests in 0.9% CO. CO-CFP expression (percent CS+ intake) was significantly but marginally reduced by scopolamine (70%), mecamylamine (85%) and baclofen (74%) relative to vehicle (98%). CO-CFP acquisition was eliminated (41%) by scopolamine relative to vehicle (88%) and limited control (98%) conditions. Neither mecamylamine nor baclofen altered CO-CFP acquisition. Thus, the muscarinic cholinergic receptor system is essential for acquisition (learning) of both fat-induced and sugar (fructose)-induced preferences. In contrast, muscarinic, nicotinic and GABA receptors were minimally involved in the expression (maintenance) of fat- and fructose-CFP.