Changes in synaptosomal ectonucleotidase activities in two rat models of temporal lobe epilepsy

Abstract

Adenosine has been proposed as an endogenous anticonvulsant which can play an important role in seizure initiation, propagation and arrest. Besides the release of adenosine per se, the ectonucleotidase pathway is an important metabolic source of extracellular adenosine. Here we evaluated ATP diphosphohydrolase and 5′-nucleotidase activities in synaptosomes from hippocampus and cerebral cortex at different periods after induction of status epilepticus (SE) by intraperitoneal administration of pilocarpine or kainate. Ectonucleotidase activities from synaptosomes of hippocampus and cerebral cortex of rats were significantly increased at 48–52 h, 7–9 days and 45–50 days after induction of SE by pilocarpine. In relation to kainate model, both hippocampal enzymes were enhanced at 7–9 days and 45–50 days, but only 5′-nucleotidase remained elevated at 100–110 days after the treatment. In cerebral cortex, an increase in ATP diphosphohydrolase was observed at 48–52 h, 7–9 days and 45–50 days after induction of SE by kainate. However, 5′-nucleotidase activity only presented significant changes at 45–50 and 100–110 days. Our results suggest that SE can induce late and prolonged changes in ectonucleotidases activities. The regulation of the ectonucleotidase pathway may play a modulatory role during the evolution of behavioral and pathophysiological changes related to temporal lobe epilepsy.