To test the hypothesis that altered GABA synthesis within nucleus reticularis thalami (NRT) neurons regulates absence seizures, we analyzed and quantitated the distribution of GAD(67) and GAD(65), the rate-limiting enzymes of GABA synthesis, in thalamic nuclei from the Cacnb4lh model of absence seizures and non-epileptic (+/+) controls. In situ hybridization and Western blot results indicate a significant increase in GAD(67) expression (mRNA and protein) per cell but no change in GAD(65) in Cacnb4lh mice. These data suggest that GABA-synthesis is maintained or increased in NRT neurons in the Cacnb4lh mouse model.
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