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.