Metabolic Approach to Evaluate Neuroprotection Promoted by A1 Adenosine Agonist in Pilocarpine-induced Epilepsy. / Abordagem Metabólica na Avaliação da Neuroproteção Promovida pelo Agonista Adenosinérgico A1 no Modelo de Epilepsia Induzida por Pilocarpina.

AUTOR(ES)

Iara Ribeiro Silva

DATA DE PUBLICAÇÃO

2009

RESUMO

It is well known that the mismatch between local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) are frequently associated with seizure-induced neuronal damage in adult animal. This study was performed to verify if the neuroprotective effect of adenosinergic A1 receptor agonist R-Pia injected prior to pilocarpine could modulate LCGU and LCBF during status epilepticus (SE). Four groups were studied: Saline, RPia+ Saline, Pilo and R-Pia+Pilo. For the LCGU and LCBF determinations, rats were subjected to autoradiographic methods using [14C]-2-deoxyglucose and [14C]-iodoantypirine, respectively, and studied 4 hours after SE onset. Neurodegeneration was evaluated at acute, latent and chronic period by Fluorojade-B method. The results showed significant hypermetabolism in almost all studied areas of Pilo and R-Pia+Pilo group compared to control values. The R-Pia+Pilo group presented differential hypermetabolism in several regions, with less intense rates in substantia nigra pars reticulata (-67.96%, p <0.001) and dentate gyrus (-54.01%, p <0.001) compared to Pilo group. Besides, significant increases in LCBF were observed in all brain areas of the experimental groups compared to control group. The increases of LCBF was more intense in rats from R-Pia+Pilo group compared to Pilo group, and was located mainly in the hippocampal formation (p<0.05); thalamus (P <0.05); entorhinal cortex (P <0.05) and mammillary body (P <0.05). These results showed that R-Pia neuroprotective effect in hippocampus, piriform cortex and basolateral amygdala, at different periods (acute, latent and chronic) demonstrated by Fluoro Jade B method was accompanied by compensatory metabolic equilibration in brain areas involved with seizures. Our quantitative autoradiographic studies show that R-Pia induces a decrease in the imbalance between glucose consumption and local blood flow during status epilepticus and this effect could represent a compensatory mechanism resulting in neuroprotection.

ASSUNTO(S)

1. epilepsia. 2. pilocarpina. 3. metabolismo da glicose cerebral. 4. fluxo sanguíneo cerebral. 5. neuroproteção. 6. adenosina. neurologia

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