Baclofen differentially mediates fructose-conditioned flavor preference and quinine-conditioned flavor avoidance in rats

Rats display both fructose-conditioned flavor preference (CFP) and quinine conditioned flavor avoidance (CFA). Dopamine (D1 and D2), muscarinic and nicotinic, but not NMDA or opioid receptor antagonists reduced fructose-CFP expression. Dopamine D1, dopamine D2, muscarinic or NMDA, but not opioid or nicotinic receptor antagonists reduced fructose-CFP acquisition. Dopamine D1, NMDA, nicotinic or opioid, but not dopamine D2 or muscarinic receptor antagonists enhanced quinine-CFA acquisition. Baclofen (BAC), a GABAB receptor agonist, alternately enhances or reduces feeding under specific conditions. The present study examined whether systemic BAC administration mediated fructose-CFP expression and acquisition or quinine-CFA acquisition. Fructose-CFP expression studies trained rats with one flavor (CS+) in 8% fructose and 0.2% saccharin and a second (CS−) flavor in 0.2% saccharin, followed by vehicle (VEH) and BAC (0.5–5mg/kg) preceding 2-bottle (CS+, CS−) 0.2% saccharin choice tests. Fructose-CFP acquisition studies administered VEH or BAC (3 or 5mg/kg) prior to CS+ and CS− training sessions followed by six 2-bottle (CS+, CS−) 0.2% saccharin choice tests. Quinine-CFA acquisition studies administered VEH or BAC (3 or 5mg/kg) prior to CS− (8% fructose+0.2% saccharin) and CS+ (fructose+saccharin+0.030% quinine) training sessions followed by six 2-bottle (CS−, CS+) fructose+saccharin choice tests. BAC (3mg/kg) minimally (66%) reduced fructose-CFP expression. BAC failed to alter fructose-CFP acquisition. Quinine-CFA acquisition was enhanced by the 5mg/kg BAC dose (15–25%) relative to VEH (34–48%). These data implicate GABAB receptor signaling in acquisition of quinine avoidance with minimal or no effects upon fructose preferences.