Sigma-1 receptor antagonismpromotes long-trace ethanolinduced conditioned tasteaversion in adolescent rats

• Salguero, Agustín ^[2] ; Mujica, Victoria ^[2] ; Ruiz-Leyva, Leandro ^[3] ; Morón Henche, Ignacio ^[1] ; Cendán, Cruz Miguel ^[3] ; Marengo, Leonardo ^[2] ; Moreno, Paloma ^[2] ; Pautassi, Ricardo ^[2]
  1. [1] Universidad de Granada

     Universidad de Granada

     Granada, España

     
  2. [2] Instituto de Investigación Médica M. y M. Ferreyra (INIMEC –CONICET-Universidad Nacional de Córdoba)
  3. [3] Department of Pharmacology, Institute of Neuroscience, Biomedical Research Center (CIBM) Faculty of Medicine, University of Granada, Spain

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• Localización: Revista Argentina de Ciencias del Comportamiento ( RACC ), ISSN-e 1852-4206, Vol. 16, Nº. Extra 3 (Suplemento (Septiembre)), 2024 (Ejemplar dedicado a: Actas de resúmenes de la XIX Reunión Nacional y VIII Encuentro Internacional de la Asociación Argentina de Ciencias del Comportamiento), págs. 149-150
• Idioma: inglés
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  • Introduction:Previous studies suggest that the Sigma receptor system is involved in the motivational effects of ethanol. Objective:we examined, in adolescent rats, the involvement of the sigma 1 receptor (S1-R) antagonist S1RA in an ethanol-induced conditioned taste aversion (CTA). Methods: we studied the role of S1RA in an ethanol-induced 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. Results:In Experiment 1we 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 alcoholat 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 notexhibit 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. Discussion: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.