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• W2017067141 abstract "gamma-Aminobutyric acid (GABA) is synthesized in brain in at least two compartments, commonly called the transmitter and metabolic compartments, and because regulatory processes must serve the physiologic function of each compartment, the regulation of GABA synthesis presents a complex problem. Brain contains at least two molecular forms of glutamate decarboxylase (GAD), the principal synthetic enzyme for GABA. Two forms, termed GAD65 and GAD67, are the products of two genes and differ in sequence, molecular weight, interaction with the cofactor, pyridoxal 5'-phosphate (pyridoxal-P), and level of expression among brain regions. GAD65 appears to be localized in nerve terminals to a greater degree than GAD67, which appears to be more uniformly distributed throughout the cell. The interaction of GAD with pyridoxal-P is a major factor in the short-term regulation of GAD activity. At least 50% of GAD is present in brain as apoenzyme (GAD without bound cofactor; apoGAD), which serves as a reservoir of inactive GAD that can be drawn on when additional GABA synthesis is needed. A substantial majority of apoGAD in brain is accounted for by GAD65, but GAD67 also contributes to the pool of apoGAD. The apparent localization of GAD65 in nerve terminals and the large reserve of apoGAD65 suggest that GAD65 is specialized to respond to short-term changes in demand for transmitter GABA.(ABSTRACT TRUNCATED AT 250 WORDS)" @default.
• W2017067141 created "2016-06-24" @default.
• W2017067141 creator A5007642133 @default.
• W2017067141 creator A5079801176 @default.
• W2017067141 date "1993-02-01" @default.
• W2017067141 modified "2023-09-26" @default.
• W2017067141 title "Regulation of ?-Aminobutyric Acid Synthesis in the Brain" @default.
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