TY - JOUR
T1 - Baclofen differentially mediates fructose-conditioned flavor preference and quinine-conditioned flavor avoidance in rats
AU - Rotella, Francis M.
AU - Vig, Vishal
AU - Olsson, Kerstin
AU - Pagirsky, Jeremy
AU - Aminov, Alon
AU - Kohen, Ilanna
AU - Bodnar, Richard J.
N1 - Publisher Copyright:
© 2016 Elsevier B.V. All rights reserved.
PY - 2016/3/15
Y1 - 2016/3/15
N2 - 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 (0.5-5 mg/kg) preceding 2-bottle (CS+, CS-) 0.2% saccharin choice tests. Fructose-CFP acquisition studies administered VEH or BAC (3 or 5 mg/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 5 mg/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 (3 mg/kg) minimally (66%) reduced fructose-CFP expression. BAC failed to alter fructose-CFP acquisition. Quinine-CFA acquisition was enhanced by the 5 mg/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.
AB - 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 (0.5-5 mg/kg) preceding 2-bottle (CS+, CS-) 0.2% saccharin choice tests. Fructose-CFP acquisition studies administered VEH or BAC (3 or 5 mg/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 5 mg/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 (3 mg/kg) minimally (66%) reduced fructose-CFP expression. BAC failed to alter fructose-CFP acquisition. Quinine-CFA acquisition was enhanced by the 5 mg/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.
KW - Conditioning
KW - GABA receptor
KW - Learning
UR - http://www.scopus.com/inward/record.url?scp=84959328805&partnerID=8YFLogxK
U2 - 10.1016/j.ejphar.2016.02.015
DO - 10.1016/j.ejphar.2016.02.015
M3 - Article
C2 - 26852956
AN - SCOPUS:84959328805
SN - 0014-2999
VL - 775
SP - 15
EP - 21
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
ER -