GABA-TGlutamic Acid Decarboxylase and GABA Transaminase
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MEIF (200 and 400 mg/kg, p.o.) attenuated the PTZ-induced increase in the activity of GABA-T in the rat brain.
In addition, it has also been reported that PTZ increases the level of GABA-T in the brain 40].
PTZ significantly increased the level of GABA-T activity in the rat brain.
Glutamic acid decarboxylase (GAD) and y-aminobutyric acid transaminase (GABA-T) are the GABA synthesizing and metabolizing enzymes, respectively (Sherif and Ahmed 1995).
The content of the neurotransmitter GABA in the central nervous system of the mammalian brain is related to the available amounts of GAD, GABA-T, and other enzymes (Sherif and Ahmed 1995).
to inhibit GABA-T activity (Awad et al., 2007; Awad et al., 2009) and increase the availability of GABA in the brain, we hypothetized that Melissa officinalis L.
GABAergic properties, through inhibition of gamma-aminobutyric acid transaminase (GABA-T).
Attempts to correlate alterations in brain GABA metabolism by GABA-T inhibitors with their anticonvulsant effects.
Only two patients have been described with GABA-T deficiency.
Several methods for measuring GABA-T activity have been published (9-11), but all of these methods are indirect, nonspecific, and/or not sensitive enough to be used in a crude tissue preparation.
GABA-T was isolated from rat brain according to the procedure of Churchich and Moses (1981) with some modifications.
GABA-T activity was assayed using a modified procedure of Qiu et al.