Abstract

To investigate the possible role of N- methyl- d-aspartate (NMDA) receptors in the seizures of E1 mice, a genetic animal model of epilepsy, we measured [ 3H]3-[(+)-2-(carboxypiperazin-4-yl)][1,2- 3H]-propyl-1-phosphonic acid (CPP) binding in several brain regions of E1 and ddY mice. At 22–24 weeks of age, the maximum number of binding sites ( B max ) of [ 3H]CPP was lower only in the cerebral cortex of both stimulated and unstimulated El mice (El(+) and El(−), respectively) than in that of ddY mice. A reduction in B max values of cortical [ 3H]CPP binding of E1 mice was detected after the age of 12 weeks. Cortical [ 3H]CPP binding in El(+) mice decreased further transiently after evoked seizures. No significant change was observed in El(−) mice after postural stimulation. These results suggest that El(+) and El(−) mice share seizure propensity and that activation of NMDA receptors is involved in the seizures of E1 mice.

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