Dopamine D1 and opioid receptor antagonism effects on the acquisition and expression of fat-conditioned flavor preferences in BALB/c and SWR mice

Sugar and fat appetites are influenced by unlearned and learned responses to orosensory and post-ingestive properties which are mediated by dopamine (DA) and opioid transmitter systems. In BALB and SWR mice, acquisition and expression of sucrose conditioned flavor preferences (CFP) are differentially affected by systemic DA D1 (SCH23390: SCH) and opioid (naltrexone: NTX) antagonism. The present study examined whether fat-CFP occurred in these strains using preferred (5%) and less preferred (0.5%) Intralipid solutions, and how SCH and NTX altered its expression and acquisition. Food-restricted mice drank flavored (CS +, e.g., cherry) 5% and flavored (CS −, e.g., grape) 0.5% Intralipid solutions in alternate 1 h/day sessions. Six two-bottle tests with both CS flavors presented in 0.5% Intralipid occurred. Robust and comparable fat-CFP was observed in both strains. In Experiment 2, vehicle (Veh), SCH (50-800 nmol/kg) or NTX (1-5 mg/kg) were administered prior to two-bottle testing in an identical paradigm. Expression of fat-CFP was significantly reduced by SCH and NTX in BALB mice, and only by SCH in SWR mice. NTX produced significantly greater inhibition of fat-CFP expression in BALB versus SWR mice. In Experiment 3, separate groups of BALB and SWR mice received Veh, SCH (50 nmol/kg) or NTX (1 mg/kg) injections prior to daily one-bottle CS + and CS − training sessions to assess acquisition effects. Six two-bottle CS + vs. CS − choice tests were then conducted. Fat-CFP acquisition was significantly reduced in SWR mice by SCH, but not NTX, and was only mildly affected by both antagonists in BALB mice. SCH produced significantly greater inhibition of fat-CFP acquisition in SWR versus BALB mice. The pattern of SCH effects upon the expression and acquisition of fat-CFP in BALB and SWR mice was quite similar to that observed for sucrose-CFP, suggesting similar DA D1 receptor involvement in sugar- and fat-CFP in these mouse strains.