Altered ATP hydrolysis induced by pentylenetetrazol kindling in rat brain synaptosomes

The ectonucleotidase pathway is an important metabolic source of extracellular adenosine. Adenosine has potent anticonvulsant effects on various models of epilepsy. One of these models is pentylenetetrazol (PTZ) kindling, in which repeated administration of subconvulsive doses of this drug induces p...

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Detalles Bibliográficos
Autores: Bonan, Carla Denise, Amaral, Olavo Bohrer, Rockenbach, Isabel Cristina, Walz, Roger, Battastini, Ana Maria Oliveira, Izquierdo, Ivan Antonio, Sarkis, João José Freitas
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2000
País:Brasil
Institución:Universidade Federal do Rio Grande do Sul (UFRGS)
Repositorio:Repositório Institucional da UFRGS
Idioma:inglés
OAI Identifier:oai:www.lume.ufrgs.br:10183/218298
Acceso en línea:http://hdl.handle.net/10183/218298
Access Level:acceso abierto
Palabra clave:Adenosina
Epilepsia
Excitação neurológica
Pentilenotetrazol
Ectonucleotidases
Adenosine
Epilepsy
Kindling
Pentylenetetrazol
Descripción
Sumario:The ectonucleotidase pathway is an important metabolic source of extracellular adenosine. Adenosine has potent anticonvulsant effects on various models of epilepsy. One of these models is pentylenetetrazol (PTZ) kindling, in which repeated administration of subconvulsive doses of this drug induces progressive intensification of seizure activity. In this study, we examine the effect of a single convulsive injection (60 mg/kg, i.p.) or 10 successive (35 mg/kg, i.p.) injections of PTZ on synaptosomal ectonucleotidases. Our results have shown that no changes in ectonucleotidase activities were seen at 0, 1, and 24 h or at 5 days after a single convulsive PTZ injection. However, after PTZ-kindling, rats which were more resistant to seizure development presented an increase in ATP hydrolysis in synaptosomes from hippocampus and cerebral cortex (44% and 28%, respectively). These results suggest that changes in nucleotide hydrolysis may represent an important mechanism in the modulation of chronic epileptic activity in this model.