Glutamate decarboxylase isoforms in thalamic nuclei in lethargic mouse model of absence seizures.
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.
Lin
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Departments of Medicine (Neurology) and Neurobiology, Epilepsy Research Laboratory, Duke University and Veterans Administration Medical Centers, Bldg. 16, Rm. 38, 508 Fulton St., Durham, NC, 27705, USA.
Lin
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Wang
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Hosford
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D000818:Animals; D015220:Calcium Channels / Q000235:genetics; D004195:Disease Models, Animal; D004832:Epilepsy, Absence / Q000201:enzymology* / Q000235:genetics*; D005968:Glutamate Decarboxylase / Q000235:genetics* / Q000378:metabolism*; D017403:In Situ Hybridization; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D007700:Kinetics; D051379:Mice; D008818:Mice, Neurologic Mutants; D013787:Thalamic Nuclei / Q000378:metabolism*
C491530:Cacnb4 protein, mouse; D015220:Calcium Channels; D007527:Isoenzymes; D005968:Glutamate Decarboxylase