| First Author | Shimura T | Year | 2004 |
| Journal | Neurosci Lett | Volume | 356 |
| Issue | 3 | Pages | 171-4 |
| PubMed ID | 15036622 | Mgi Jnum | J:107583 |
| Mgi Id | MGI:3621507 | Doi | 10.1016/j.neulet.2003.11.041 |
| Citation | Shimura T, et al. (2004) Altered taste function in mice deficient in the 65-kDa isoform of glutamate decarboxylase. Neurosci Lett 356(3):171-4 |
| abstractText | The 65-kDa isoform of glutamate decarboxylase (GAD65) is considered to play an important role for GABA synthesis in the central nervous system. Using mice with targeted ablation of the GAD65 gene (GAD65(-/-) mice) we investigated a possible involvement of GABAergic neurotransmission in several taste functions. Preference/aversion responses to four basic tastes were not different between GAD65(-/-) and wild-type mice during a 48-h two-bottle choice test. GAD65(-/-) mice consumed less sucrose-quinine mixtures than did wild-type mice. The injection of midazolam (5 mg/kg), a benzodiazepine agonist, significantly increased the consumption of 100 mM sucrose in the wild-type mice. The same injection, however, failed to increase intake of the 100 mM sucrose in GAD65(-/-) mice. These results suggest that GAD65-generated GABA is not implicated in basic taste functions such as simple detection and discrimination. Rather, more complex processing of taste information including taste mixtures and palatability may be finely tuned by GAD65-mediated GABA synthesis. |
