IFEC   20925
INSTITUTO DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
“Involvement of the Glutamatergic Neurotransmission in the Stress and Cocaine-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in rats”
Autor/es:
DE GIOVANNI, LAURA, ; VIRGOLINI, MIRIAM BEATRIZ; CANCELA, LILIANA
Lugar:
Huerta Grande , Cordoba,
Reunión:
Workshop; IIRCN- Second Join Meeting of the Argentine Society for Neurociences (SAN) and the Argentine Workshop in Neurosciences; 2010
Institución organizadora:
Sociedad Argentina de Neurociencia y Taller Argentino de Neurociencia
Resumen:
Involvement of Glutamatergic Neurotransmission in the Stress and Cocaine-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in rats   De Giovanni, Laura Noemi; Virgolini, Miriam Beatriz, Cancela, Liliana Marina. luli_deyo@yahoo.com.ar Previous results from our lab showed that MK 801 abrogated the development and the expression of the stress-induced reinstatement (SR), in extinguished cocaine-induced conditioned place preference (CPP) in rats, and that this was context-dependent and persistently observed on subsequent cocaine-induced reinstatements (CR). Our goal was to determine if the reconsolidation memory process could be involved in the long lasting blockade of MK-801 on CR. Male Wistar rats (220-300g) were conditioned with cocaine (10-mg/kg ip) during four alternated drug/vehicle sessions and later extinguished with successive vehicle associations. In the reinstatement day, a group of animals was 30 min-immobilized, and control group was no exposed to stress. Subsequently, all groups were tested in the CPP and, immediately or 3 h after, injected with MK 801 (0.1 mg/kg ip) or vehicle, and 3 days after evaluated for CR. MK 801 administered immediately after SR blocked the CR, whereas the reinstatement showed up in the animals injected 3 h after the test. The long-term blockade of CR by the glutamatergic neurotransmission antagonism immediately after the first reinstatement, could be attributed to a disruption of the reconsolidation memory process of the cocaine-induced CPP