Chronic Seizures Increase Glucose Transporter Abundance in Rat Brain

Pentylenetetrazole and kainic acid, seizure-inducing agents that are known to increase glucose utilization in brain, were used to produce chronic seizures in mature rats. To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression...

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Bibliographic Details
Published in:Journal of neuropathology and experimental neurology 1996-07, Vol.55 (7), p.832-840
Main Authors: Gronlund, Kathryn M, Gerhart, David Z, Leino, Richard L, Mccall, Anthony L, Drewes, Lester R
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Brain - drug effects
Brain - metabolism
Chronic Disease
Glucose Transporter Type 1
Glucose Transporter Type 3
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Immunoblotting
Immunohistochemistry
Kainic Acid - pharmacology
Male
Medical sciences
Monosaccharide Transport Proteins - metabolism
Nerve Tissue Proteins
Nervous system (semeiology, syndromes)
Neurology
Pentylenetetrazole - pharmacology
Rats
Rats, Sprague-Dawley
Reference Values
Seizures - metabolism
Time Factors
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Summary:Pentylenetetrazole and kainic acid, seizure-inducing agents that are known to increase glucose utilization in brain, were used to produce chronic seizures in mature rats. To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression, polyclonal carboxyl-terminal antisera to glucose transporters (GLUT1 and GLUT3) were employed with a quantitative immunocytochemical method and immunoblots to detect changes in the regional abundances of these proteins. GLUT3 abundances in control rats were found to be correlated with published values for regional glucose utilization in normal brain. Following treatment with kainic acid and pentylenetetrazole, both GLUT3 and GLUT1 increased in abundance in a region and isoform-specific manner. GLUT3 was maximal at eight hours, whereas GLUT1 was maximal at three days. Immunoblots indicated that most of the GLUT3 increase was accounted for by the higher molecular weight component of the GLUT3 doublet. The rapid response time for GLUT3 relative to GLUT1 may be related to the rapid increase in neuronal metabolic energy demands during seizure. These observations support the hypothesis that glucose transporters may be upregulated in brain under when brain glucose metabolism is elevated.
ISSN:0022-3069
1554-6578
DOI:10.1097/00005072-199607000-00008