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PubMed1979

GABA transaminase inhibitors.

In summary, several branched-chain fatty acids appeared to be competitive inhibitors of GABA-T and non-competitive inhibitors of SSADH. These compounds produce an increase in brain GABA level, and for two of these it was shown that the increase differs among various brain areas. An increase of GABA cannot be obtained by inhibition of SSADH. The increase in brain GABA seems to correlate with the anticonvulsant activity of branched-chain fatty acids.

4-Aminobutyrate Transaminase↗
PubMed1979

Inhibition of isolation-induced aggressive behavior with GABA transaminase inhibitors.

Administration of aminooxyacetic acid (AOAA) and gamma-acetylenic GABA (GAG) resulted in a dose-dependent suppression of aggressive behavior and a concomitant increase in brain GABA. The increase in GABA levels persisted beyond the time when AOAA and GAG exerted an anti-aggressive effect. Brain GABA levels remained significantly elevated over controls for 120 h after a single injection of AOAA and 46 h after a single dose of GAG.

4-Aminobutyrate Transaminase↗
PubMed1981

The influence of a GABA transaminase inhibitor, gamma-vinyl GABA, on voluntary morphine consumption in the rat.

Morphine-dependent and control rats in an oral free-choice protocol were treated with gamma-vinyl GABA (GVG), 60, 120 and 240 mg/kg IP, for 3 days over three successive periods. Morphine dependence was assessed with naltrexone. Fluid intake of morphine-dependent rats was reduced during GVG treatment and the proportion of fluid taken as morphine was also decreased, but not sufficiently to induce withdrawal signs. Intake by controls was only affected by 240 mg/kg GVG, when body weight decreased. The attentuation of morphine consumption by GVG treatment may, within the limitations of this protocol, interfere with the positive reinforcing properties of morphine.

4-Aminobutyrate Transaminase↗