IFEC   20925
INSTITUTO DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Influence of chronic restraint stress on cocaine-induced glutamate release in the nucleus accumbens
Autor/es:
GARCIA KELLER, C; AVALOS M.P; CANCELA L.M.; BOLLATI, F.; GUZMAN, A.S.; RIGONI, D.
Lugar:
Mar del plata
Reunión:
Congreso; XXXII Congreso de la Sociedad Argentina de Investigación en Neurociencias; 2017
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencias
Resumen:
Influence of chronicrestraint stress on cocaine-induced glutamate release in the nucleus accumbensGuzman*, AndreaS.; Avalos*, María P.; Garcia-Keller, Constanza; Bollati, Flavia; Cancela,Liliana M. IFEC-CONICET,Departamento de Farmacología, Facultad de Ciencias Químicas, UniversidadNacional de Córdoba, Córdoba, Argentina*equal contribution Cross-sensitization between stress and drugs ofabuse may be explained by long-term neurobiological changes in themesocorticolimbic dopamine (DA) and glutamate (GLU) transmissions;specifically, within Nucleus Accumbens (NAc), the major limbic-motorintegration area. In this sense, previous results from our lab havedemonstrated that after two weeks of a single exposure to restraint stress achallenge of cocaine induced locomotor sensitization and a parallel increase inextracellular DA levels in Core compartment of NAc, meanwhile GLU levels inthis area were not modified. The present study attempted to determinate thelong-term effect of chronic restraint stress pre-exposure in extracellularlevels of GLU in NAc Core in response to cocaine. Wistar rats were exposed to repeated(2h for 7 days) restraint stress and two weeks after the last stress session,all animals were implanted with probes of microdialysis in NAc Core. The dayafter surgery, GLU dialysate samples were collected and quantified by HPLC.After cocaine administration (15 mg/kg, i.p.), animals pre-exposed to chronic stressdid not show increased extracellular glutamate levels in NAc Core, similarly toour results obtained following pre-exposure to acute stress. These findingscould be explained in the framework of a dysregulation of GLU homeostasisinduced by stress. The current study provides neurochemical basis in order toinvestigate the mechanisms underpinning the comorbidity between stress and drugabuse