Sigma-1 receptor antagonism promotes long-trace ethanol induced conditioned taste aversion in adolescent

A SALGUERO; MUJICA V; IGNACIO MORÓN HENCHE; CENDAN C; MORENO PALOMA; MARENGO, L.; PAUTASSI R.M.

Congreso; 19a Reunión Nacional y 8vo Encuentro Internacional de la Asociación Argentina de Ciencias del Comportamiento; 2023

Asociación Argentina de Ciencias del Comportamiento

Sigma-1 receptor antagonism promotes long-trace ethanol-induced conditioned taste aversion in adolescent ratsAgustín Salgueroa,*; Victoria Mujicaa; Leandro Ruiz-Leyvab; Ignacio Morón Henchec; Cruz Miguel Cendánb,d ; Leonardo Marengoa,; Paloma Morenoa & Ricardo Pautassia,daInstituto de Investigación Médica M. y M. Ferreyra (INIMEC – CONICET-Universidad Nacional de Córdoba), Córdoba, 5000, ArgentinabDepartment of Pharmacology, Institute of Neuroscience, Biomedical Research Center (CIBM) Faculty of Medicine, University of Granada, SpaincDepartment of Psychobiology and Centre of Investigation of Mind, Brain, and Behavior (CIMCYC), Faculty of Psychology, University of Granada, SpaindFacultad de Psicología, Universidad Nacional de Córdoba, Córdoba, Argentina*Agustín Salguero; Email: asalguero@immf.uncor.edu Previous studies suggest that the Sigma receptor system is involved in the motivational effects of ethanol. We examined, in adolescent rats, the involvement of the sigma 1 receptor (S1-R) antagonist S1RA in an ethanol-induced conditioned taste aversion (CTA) in which the Conditioned Stimulus (CS, saccharine, 0.1%) was presented immediately before the Unconditioned Stimulus (US, ethanol, 2.5 g/kg) or with a CS-US interval of 30 minutes. In Experiment 1 we found that administration of S1RA (4 or 16 mg/kg, administered 30 min before alcohol) did not alter the expression or extinction of ethanol-induced CTA. A second phase of this experiment tested control rats (i.e., those administered with 0 g/kg alcohol at the previous phase) for lithium-chloride–induced CTA (like in the previous phase, the CS was presented immediately before the US), which was not affected by S1RA (16 mg/kg). In Experiment 2 we inserted a 30 min interval between CS and US, and this resulted in the absence of ethanol-induced CTA. Administration of S1RA (16 mg/kg) before alcohol, however, promoted the expression of this long-trace ethanol-induced CTA at adolescence. Intriguingly, we found that rats given S1RA at conditioning (PD30) did not exhibit ethanol-induced locomotor activity, when assessed later at adolescence (PD39). Administration of S1RA (16 mg/kg) did not affect mean alcohol blood levels at PD30. These results suggest that S1-R antagonism, at adolescence, might block the appetitive effects of ethanol and, therefore, exacerbate the aversive effects of this drug.