Abstracts

Objective: In the present study we investigated the alterations in D2-like dopamine receptor binding and the activation of Gi protein that is coupled to these receptors in an experimental model of epilepsy. Methods: In male Wistar rats used as control and kindled (epileptic) group (n=8, each), it was evaluated D2-like dopaminergic receptor binding and [35S] GTP S incorporation due to activation of D2-like receptors in different brain areas associated with epileptic activity, ipsi- and contralateral to the epileptic focus. Results: It was observed a reduction in the D2-like dopaminergic receptor binding in striatum (25 and 35 %, ipsi- and contralateral) and contralateral nucleus accumbens (39 %) in kindled animals. However, there was an increase in the activation to Gi protein associated to D2-like dopaminergic receptor in striatum (91-121%); nucleus accumbens (88-112%); amygdala (46-62%); entorhinal (52%), temporal (51-62%) and sensorimotor cortex (54-78%); sustantia nigra (31%), dorsal (56%) and ventral CA1 (30-34 %), ventral CA2 (63 %), ventral CA3 (30 %) and ventral dentate gyrus (25-28 %). Conclusion. Despite there is a decrease in the D2-like dopaminergic receptor binding, it exist an increase in the activation of Gi protein coupled to these receptors. This results suggest a hypersensitivity to Dopamine effects mediated by D2-like dopamine receptors in the epileptic brain. Suported by CONACYT No. 98386; scholarship from CONACYT No. 203803.