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In. II International Congress on Neuroregeneration. Proceedings (selected papers). Rio de Janeiro, UFRJ, 2004. p.127-131, tab.
Monografia em Inglês | LILACS | ID: lil-682601

RESUMO

Recently published data (Baran et al., Neurosignals 2004; 13: 290-7) have shown significantly increased activity of glutamic acid decarboxylase, the neuronal marker for gamma-aminobutyrate (GABA)-neurons, in the frontal cortex of rat brains, 6 months after kainic acid (KA) injection. In present study glutamate and GABA levels in the frontal cortex of rats in the KA (10 mg/kg, subcutaneously)-induced spontaneous recurrent seizure model of epilepsy, 6 months after the initial KA-induced seizures, were investigated. Six months after KA injection there was found a slightly reduced glutamate level in the frontal cortex (89.7 % of control), whereas the GABA level was moderately increased (119.6 % of control). The ratio GABA:glutamate level was significantly increased in the frontal cortex (134.5 % of control; P<0.001). Obtained data would indicate an enhancement of GABAergic activities in the frontal cortex in the chronic KA epileptic model. Interaction within GABAergic parameters, thus the GABAA receptors, the GABAB receptors, glutamate and GABA transporters may play a role in the modulation but also in the exertion of epileptic events in chronic KA epileptic model, which needs to be clarified.


Assuntos
Animais , Ratos , Epilepsia , Epilepsia do Lobo Temporal , Ácido gama-Aminobutírico , Glutamatos , Ácido Caínico , Neurologia , Fármacos Neuroprotetores , Córtex Pré-Frontal , Receptores de GABA , Receptores de Ácido Caínico , Ratos , Ratos Sprague-Dawley
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