| First Author | Wu H | Year | 2007 |
| Journal | Brain Res | Volume | 1154 |
| Pages | 80-3 | PubMed ID | 17482148 |
| Mgi Jnum | J:122501 | Mgi Id | MGI:3714556 |
| Doi | 10.1016/j.brainres.2007.04.008 | Citation | Wu H, et al. (2007) Role of glutamate decarboxylase (GAD) isoform, GAD(65), in GABA synthesis and transport into synaptic vesicles-Evidence from GAD(65)-knockout mice studies. Brain Res 1154:80-3 |
| abstractText | In GAD(65)-knockout mice, lack of GAD(65) expression was confirmed. The expression level of vesicular GABA transporter (VGAT) was upregulated, and no change in the synaptic vesicles (SV)-associated GAD(67) was found. GAD(65)(-/-) SV transported cytosolic GABA much more efficiently than that of the wild type, further supporting our model that there is a structural and functional coupling between GABA synthesis and packaging into SV. Both full-length and truncated forms of GAD(65) could bind to GABAergic SV, indicating the N-terminus is not required for the anchoring of GAD(65) to SV. Although both GAD(65)(-/-) SV reconstituted with either GAD(65) or GAD(67) could synthesize GABA from [(3)H] glutamate and transport this newly synthesized GABA into SV, the combined evidence suggests that GAD(65) plays a major role in GABA transmission in normal physiological condition. However, GAD(67) could serve this role under some pathological conditions. |
