Rat GAD2 (Glutamate Decarboxylase 2, Acid) ELISA Kit

Mutations in the coding region of the WFS1 gene cause Wolfram syndrome, a rare multisystem neurodegenerative disorder of autosomal recessive inheritance. In clinical studies a relation between mutations in the Wfs1 gene and increased susceptibility for mood disorders has been established. According to our previous studies, mice lacking Wfs1 gene displayed increased anxiety in stressful environment. As the GABA-ergic system plays a significant role in the regulation of anxiety, we analyzed the expression of GABA-related genes in the forebrain structures of wild-type and Wfs1-deficient mice. Experimentally naive Wfs1-deficient animals displayed a significant down-regulation of alpha 1 (Gabra1) and alpha 2 (Gabra2) subunits of GABA(A) receptors in the temporal lobe and frontal cortex. Exposure of wild-type mice to the elevated plus-maze decreased levels of Gabra1 and Gabra2 genes in the temporal lobe. A similar tendency was also established in the frontal cortex of wild-type animals exposed to behavioral test. In Wfs1-deficient mice the elevated plus-maze exposure did not induce further changes in the expression of Gabra1 and Gabra2 genes. By contrast, the expression of Gad1 and Gad2 genes, enzymes responsible for the synthesis of GABA, was not significantly affected by the exposure of mice to the elevated plus-maze or by the invalidation of Wfs1 gene. Altogether, the present study demonstrates that increased anxiety of Wfs1-deficient mice is probably linked to reduced expression of Gabra1 and Gabra2 genes in the frontal cortex and temporal lobe. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

gamma-Aminobutyric acid (GABA) metabolism has been investigated in breaker and light red maturation stages of 'Tricia' tomatoes exposed to air, or 10% CO2 in air during storage, at 13 degrees C for 12 d, to examine whether GABA responses to elevated CO2 differ in fruit at different maturity stages. At harvest, the GABA concentration in red fruit was about a third of that in breaker fruit. The ripening of breaker stage fruit was inhibited by CO2 to a greater extent than the red fruit as judged by hue and chroma values, but the red fruit were more sensitive to development of water soaking, pitting and decay than the breaker fruit. During storage, GABA concentrations in breaker fruit decreased during storage but were usually higher in CO2 treated than air treated fruit. GABA concentrations in red fruit increased in CO2 treated fruit, but they increased and then decreased in air treated fruit over time. When CO2 treated fruit were transferred to air, GABA concentrations declined to similar levels as those found in fruit stored in air. Although glutamate decarboxylase (GAD) activity was higher in breaker than red fruit at harvest, activities in air and CO2 treated fruit were similar. GABA transaminase (GABA-T) activity was higher in red than breaker fruit, but activity declined more in CO2 than air treated fruit. Although, CO2 treatment did not affect GAD1 expression, it resulted in higher GAD2 and GAD3 expression, and to a greater extent in breaker than red fruit. No consistent effects of high CO2 conditions on the expression of GABA-T or succinic semialdehyde dehydrogenase (SSADH) genes were found. A decline in succinic semialdehyde reductase 1 (SSR1) gene expression was found only in CO2 treated red fruit, while CO2 treatment resulted in a more rapid decrease of SSR2 expression in both breaker and red fruit. The results reveal differences in GABA metabolism in breaker and red fruit in response to CO2 treatment. (C) 2010 Elsevier B.V. All rights reserved.