Glutamate decarboxylase isoforms in thalamic nuclei in lethargic mouse model of absence seizures.


Journal Article

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.

Full Text

Cited Authors

  • Lin, FH; Lin, S; Wang, Y; Hosford, DA

Published Date

  • July 1999

Published In

Volume / Issue

  • 71 / 1

Start / End Page

  • 127 - 130

PubMed ID

  • 10407195

Pubmed Central ID

  • 10407195

International Standard Serial Number (ISSN)

  • 0169-328X

Digital Object Identifier (DOI)

  • 10.1016/s0169-328x(99)00176-x


  • eng