VIRGOLINI MIRIAM BEATRIZ
Congresos y reuniones científicas
Título:
Effect of intra-core administration of a group I metabotropic receptor antagonist and group II agonist in the stress-induced reinstatement induced in extinguished cocaine-conditioned animals
Autor/es:
DE GIOVANNI, L.N.; VIRGOLINI, M.B.; CANCELA, L.M.
Lugar:
Valparaiso
Reunión:
Workshop; II International Workshop. Motivated behavior, stress and addiction. From Molecules to Behavior; 2012
Resumen:

EFFECT OF INTRA-CORE ADMINISTRATION OF A GROUP I METABOTROPIC RECEPTOR ANTAGONIST  AND GROUP II AGONIST IN THE STRESS- INDUCED REINSTATEMENT INDUCED IN EXTINGUISHED COCAINE-CONDITIONED ANIMALS

De Giovanni, L.N.; Virgolini, M.B.; Cancela, L.M.

luli_deyo@yahoo.com.ar

Previous results from our lab showed that both, the systemic or intra-core administration of the glutamatergic antagonist MK 801 blocked the stress-induced reinstatement in an extinguished cocaine-induced conditioned place preference (CPP) in rats. In the present experiments, our goal was to determine whether the metabotropic group I (mGlu I) and metabotropic group II (mGlu II) receptors, that exert a modulatory effect in the glutamatergic neurotransmission, could influence the stress-induced reinstatement in our CPP model. Male Wistar rats (220-300g) were conditioned with cocaine (10 mg/kg i.p.) during four alternated drug/vehicle sessions, and later extinguished with successive vehicle associations. On the reinstatement day, animals were microinfunded with LY 479234, a  mGlu I antagonist (0.1 or 1.0 ug/side), MPEP, amGlu II agonist (0.05 or 0.5 ug/side) or vehicle and 5 min later, assigned to a group according to the following treatments: 1) Stressed animals (SA): submitted to 30 min-restraint exposure, and 2) Control animals (CA): left undisturbed in their home cages, and then tested in the CPP. The results demonstrate that although MPEP blocked the stress induced reinstatement LY 479234 failed to disrupt it. These data suggest that mGlu I receptors (but no mGlu II) are involved in the stress induced reinstatement, probably with a mechanism shared with the ionotropic receptors.

Financial Support: FONCYT, Ministerio de Ciencia y Tecnología, CONICET and SECyT.