IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
-LACK OF CB1 RECEPTOR ON GABAERGIC NEURONS: EFFECTS IN A PHARMACOLOGICAL MODEL OF SCHIZOPHRENIA
Autor/es:
GARCIA-RINCON, DANIEL; BRUSCO, ALICIA; AGUARELES, JOSE; CALTANA, LAURA; SORIANO, DELIA; PARAISO LUNA, JUAN; GALVE ROPERH, ISMAEL
Lugar:
Córdoba
Reunión:
Congreso; SAN 2019; 2019
Institución organizadora:
Sociedad Argentina de Neurosciencia
Resumen:
Schizophrenia is a chronic and progressive mental disorder that combines avariety of clinical symptoms, including psychosis, anhedonia and cognitive deficits.Although the precise mechanisms responsible of schizophrenia development areunknown, several models demonstrate the involvement of dopaminergic,glutamatergic and gabaergic neurotransmission systems. In addition, acannabinergic hypothesis has been put forward. Endocannabinoid levels andcannabinoid receptor type one (CB1) signalling hence have been implicated inschizophrenia owing to their neuromodulatory role.The aim of this study was to evaluate the contribution of CB1 receptor onGABAergic neurons in psychosis like states using the model of acute systemicadministration of the N-Methyl-D-aspartate type ionotropic receptor (NMDAR)antagonist, MK-801 in wild type (WT) and GABA-CB1-KO mice. Locomotor activitywas measured in open field at 30, 60 and 90 minutes after injection. Locomotoractivity in vehicle-treated GABA-CB1-KO did not differ significantly from vehicletreated WT mice, however MK-801 induced hyperlocomotion persisted longer timein GABA-CB1-KO than WT littermates.This results indicate that CB1 receptors activity on GABAergic neurons protectfrom the susceptibility to generate a persistent psychotic-like response. This result,is however in contrast with the attenuation of psychotic responses observed bypharmacological CB1 antagonism or complete deletion of CB1 deletion.