Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P80404 (GABA transaminase)
 786 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of gamma-aminobutyric acid (GABA) in the control of plasma testosterone was studied on male mice of inbred strains (CBA/Lac, A/He and BALB/c) exposed to a sexually receptive female in the same cage but separated by a partition. Within 40 minutes, testosterone levels in plasma increased 1.5-3.5 times depending upon the mouse genotype. This process could be completely blocked if GABA accumulation was induced by pretreatment with the GABA transaminase inhibitor, aminooxyacetic acid (AOAA), or by emotional stress induced by 40 min of restraint. Neither bicuculline-induced blockade of GABA receptors nor a decrease of GABA concentration induced by prior administration of thiosemicarbazide (an inhibitor of glutamate decarboxylase), affected the increase of plasma testosterone that occurred in response to presentation of a receptive female. However, at sexual arousal, the bicuculline blockade of GABA receptors significantly reduced the inhibitory effects of both AOAA administration and emotional stress on plasma testosterone levels. We conclude that the inhibitory effect of emotional stress on female-induced activation of testicular endocrine function is mediated, at least in part, via activation of bicuculline-sensitive receptors.
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PMID:Gamma-aminobutyric acid controls the mouse hypothalamic-pituitary-testicular response to the presence of female. 180 32

We examined the effect of (+/-)-gamma-vinyl GABA (GVG, Vigabatrin), an irreversible inhibitor of the enzyme GABA transaminase, on the acquisition and expression of cocaine-induced sensitization in albino male Sprague-Dawley rats. Animals received a single injection of 1 ml/kg i.p. of 0.9% saline or 15 mg/kg i.p. of (-)-cocaine and locomotor activity was assessed using automated locomotor cages and stereotyped behaviors were scored using a 4-point rating scale (Day 1). Subsequently, animals were given 15 mg/kg i.p. of cocaine every 48 h in their home cage for 1 week (Days 3, 5, and 7) and then given no treatment for 1 week. A challenge injection of 15 mg/kg i.p. of cocaine, but not vehicle, produced a significant increase in locomotor activity and stereotyped behaviors on Day 15 compared to animals that received cocaine on Day 1. Administration of 75 mg/kg i.p. of GVG 2.5 h before the cocaine injections did not significantly alter the acquisition of cocaine-induced locomotor sensitization. However, 150 mg/kg i.p. of GVG significantly attenuated the acquisition of cocaine-induced locomotor sensitization. Administration of 150 mg/kg i.p. of GVG 2.5 h before the cocaine challenge injection on Day 15 significantly attenuated the expression of cocaine-induced locomotor sensitization. Acquisition and expression of cocaine-induced sensitization of stereotypy was also significantly attenuated by 150 mg/kg i.p. of GVG. Since sensitization may be one of the factors involved in relapse to drug use, the present results, in combination with previous findings that GVG blocks the rewarding and incentive motivating effects of cocaine, suggest that GVG might prove useful in the treatment of cocaine addiction.
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PMID:Gamma-vinyl GABA, an irreversible inhibitor of GABA transaminase, alters the acquisition and expression of cocaine-induced sensitization in male rats. 1237 39