CHRONIC SEIZURES INCREASE GLUCOSE-TRANSPORTER ABUNDANCE IN RAT-BRAIN

Pentylenetetrazole and kainic acid, seizure-inducing agents that are k nown to increase glucose utilization in brain, were used to produce ch ronic seizures in mature rats. To test the hypothesis that increased b rain glucose utilization associated with seizures may alter glucose tr ansporter expression, polyclonal carboxyl-terminal antisera to glucose transporters (GLUT1 and GLUT3) were employed with a quantitative immu nocytochemical method and immunoblots to detect changes in the regiona l abundances of these proteins. GLUT3 abundances in control rats were found to be correlated with published values for regional glucose util ization in normal brain. Following treatment with kainic acid and pent ylenetetrazole, both GLUT3 and GLUT1 increased in abundance in a regio n and isoform-specific manner. GLUT3 was maximal at eight hours, where as GLUT1 was maximal at three days. Immunoblots indicated that most of the GLUT3 increase was accounted for by the higher molecular weight c omponent of the GLUT3 doubler. The rapid response time for GLUT3 relat ive to GLUT1 may be related to the rapid increase in neuronal metaboli c energy demands during seizure. These observations support the hypoth esis that glucose transporters may be upregulated in brain under condi tions when brain glucose metabolism is elevated.