IFIBYNE   05513
INSTITUTO DE FISIOLOGIA, BIOLOGIA MOLECULAR Y NEUROCIENCIAS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Repetitive cocaine administration alters GABAergic thalamocortical transmission.
Autor/es:
URBANO FJ
Lugar:
Huerta Grande, Cordoba
Reunión:
Simposio; XXVII Congreso SAN 2012-Symposium I: Neurobiology of drug addiction: effects in animal models and a translational human.; 2012
Institución organizadora:
Sociedad Argentina de Investigacion en Neurociencias (SAN)
Resumen:
The goal of our lab is to study changes in the intrinsic properties of thalamocortical networks in mice exposed to cocaine. The thalamocortical system is involved in the attentional, perceptual, and sensorimotor deficits present in cocaine abusers, and is, therefore, of direct relevance to the treatment of the deleterious effects of cocaine. However, there is scant precedent of in vitro studies of either intrinsic membrane properties or changes in synaptic transmission across large numbers of thalamocortical neurons in animal models of cocaine intake. A combination of in vitro patch-clamp, calcium-dependent dyes imaging and western blotting techniques were used to determine the physiological and molecular mechanisms behind the cocaine-induced over-activation of voltage-gated calcium channels in thalamocortical networks. Acute cocaine exposure induced locomotor activity and GABAergic thalamic alterations. After systemic administration of either T-type calcium channel blockers mibefradil (20 mg/kg) or 2-octanol (0.5 mg/kg and 0.07 mg/kg) cocaineinduced hyperlocomotor activity in vivo as well as GABAergic mini frequencies enhancement onto Ventrobasal (VB) thalamic neurons were prevented. Repetitive administration of cocaine increased changes in GAD65/67 and T-type calcium channels protein levels from VB and Reticular thalamic nuclei. Our results strongly suggest that T-type calcium channels play a key role in cocaine-mediated GABAergic thalamocortical alterations, and further propose that Ttype channel blockers might represent potential targets for future pharmacological strategies aimed at treating cocaine?s deleterious effects on physiology and behavior.