| First Author | Lin FH | Year | 1999 |
| Journal | Brain Res Mol Brain Res | Volume | 71 |
| Issue | 1 | Pages | 127-30 |
| PubMed ID | 10407195 | Mgi Jnum | J:109317 |
| Mgi Id | MGI:3628706 | Doi | 10.1016/s0169-328x(99)00176-x |
| Citation | Lin FH, et al. (1999) Glutamate decarboxylase isoforms in thalamic nuclei in lethargic mouse model of absence seizures. Brain Res Mol Brain Res 71(1):127-30 |
| abstractText | 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. |
