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

gamma-Acetylenic gamma-aminobutyric acid (GAG), an irreversible inhibitor of GABA transaminase, increased the concentration of GABA in feline spinal cords to 239% of the control value by 225 min after its injection. After administration of GAG to spinally transected cats, the height of the segmentally evoked dorsal root potential (DRP), which is generated at one point via a GABA synapse, was increased to more than twice the control value although the area increased only slightly. However, GAG had no effect on the segmental DRP in the decerebrate cat. In contrast, the DRP evoked in decerebrate cats by electrical stimulation of the brain stem, which is probably mediated by GABA, was decreased by administration of GAG. These effects of GAG were accompanied by the development of spontaneous primary afferent depolarizations which resembled spontaneous DRPs in both spinal and decerebrate cats. The temporal and size correlation between spontaneous DRPs occurring in different spinal roots indicate they are generated by an interneuronal pathway that is released by the action of GAG. The action of GAG on the segmental DRP in the spinal but not decerebrate preparation is also most easily explained by GAG-induced effects on interneuronal pathways. These data suggest GABA transaminase inhibition does not affect the axoaxonic GABA synapse mediating the DRP.
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PMID:Changes in primary afferent depolarization after administration of gamma-acetylenic gamma aminobutyric acid (GAG), a gamma-aminobutyric acid (GABA) transaminase inhibitor. 50 64

In chicks with cannulae chronically implanted into the III cerebral ventricle, the effects of a single dose (10 micrograms) of beta-endorphin on GABA and free glutamic acid content, GAD and GABA-T activities in the diencephalon, brain-stem and brain hemispheres were studied at the time of maximal behavioural stuporous state and analgesia. A significant decrease in GABA concentration both in the diencephalon and brain-stem, accompanied by a significant increase in GABA-T activity in the same areas, was shown to occur. No changes were observed in GAD activity and in glutamic acid content in the studied areas of the brain. In conclusion, present experiments suggest that some central effects of a beta-endorphin may be due to an interference with GABA-ergic transmission.
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PMID:Effects of intraventricular beta-endorphin on GABA system in some areas of chick brain. 52 83

Addition of gabaculine to brain and liver extracts caused great inhibition of GABA-T activity, a much lesser but still significant inhibition of ALA-T activity, and very little inhibition of ASP-T activity. In contrast, intramuscular administration of gabaculine to mice resulted in considerable inhibition of all three enzyme activities in liver, the order of sensitivity being ALA-T greater than GABA-T greater than ASP-T. The effect of the administered gabaculine on the brain enzyme activities was more along the lines seen in the in vitro experiments but, even here, the relative sensitivities of GABA-T and ALA-T to the inhibition were much more similar than might have been predicted from the in vitro experiments.
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PMID:Inhibition of aminotransferase enzyme systems by gabaculine. 53 May 8

The effects of administration of DL-penicillamine (PeA), thiosemicarbazide (TSC), semicarbazide-HCl (SC) as convulsants and pyridoxine (PN) as anticonvulsant on gamma-aminobutyric acid (GABA) content, glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) activities in cerebral cortex, striatum, diencephalon, mesencephalon, cerebellum and pons/medulla were investigated. The onset of convulsions induced by these convulsants coincides with the fall in GABA content and GAD activity in the mesencephalon area, and in contrast, the cessation of the convulsions by PN supplement coincides with the recovery in both the parameters. Aminooxyacetic acid (AOAA), a potent GABA-elevating agent showed an anticonvulsant property against convulsion by TSC for several hours after the injection of AOAA, but lost this property 16 hr after the treatment. The TSC administration 16 hr after the AOAA pretreatment significantly decreased the GABA content in all the regions, particularly in the mesencephalon and diencephalon areas, which had been elevated by the AOAA pretreatment, together with its ability to induce convulsion. FRom the above results it may be postulated that the critical drop of GABA level from a plateau to another lower level following the decrease of GAD activity in the mesencephalon area is an important factor in the induction of convulsion.
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PMID:Effect of antivitamin B6 on regional GABA metabolism in mouse brain and its relation to convulsions. 54 51

GABA, its derivative -- gamma-hydroxybuturic acid and metabolite --succinic acid have a pronounced dilatatory activity on cerebral circulation in various brain parts. GABA increases cerebral circulation by 25.3%, gamma-hydroxybutyric acid by 35.9% and sucinic acid by 20.4%. In ischaemia of the brain a relationship has been established between cerebral circulation, changes in the GABA system in brain and in the walls of cerebral arteries. The content of GABA increases following enhancement of GAD activity and inhibition of GABA-T. The increase of endogenous GABA level in brain during hypoxia of the brain brings to an improvement of blood circulation through increasing collateral vessels. Experiments with GABA-T inhibition by aminooxyacetic acid give direct evidence about the role of the GABA system in cerebral blood circulation. This mechanism is evaluated by us as an example of an autoregulatory system that is realized by a feed-back mechanism providing the adaptability and compensatory function of cerebral haemodynamics to changing conditions.
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PMID:[Role of GABA and its derivatives in regulating cerebral circulation]. 57 37

Chronically alcoholized intoxication (1.5--2 months) induces adaptation of cerebral neurones to changing equilibrium states of biochemical processes by altering the activity of enzymes of GABA metabolism, reduction of alanine and aspartate transaminase activity and increase of LDH and succinate dehydrogenase activity. In the cerebellum and cerebral hemispheres during alcohol abstinacy the activity of GABA-T, succinate dehydrogenase and aspartate transaminase was reduced while that of LDH and alanine transaminase was increased. The administration of fusarinic acid (100 mg/kg i. p.) to control animals induced a sharp increase of GAD activity in both structures of the brain. The stimulatory effects of fusarinic acid were not observed when it was administered to animals receiving alcohol chronically. Motor activity or rats was markedly reduced during chronical alcoholism and the first days of alcohol abstinacy (24--48 h), as well as following injection fusarinic acid and homopantothenic acid. The increase of locomotion and the vertical component of motor activity was observed only following one week or one month after alcohol abstinacy.
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PMID:[Adaptive changes in brain metabolism during chronic alcoholic intoxication]. 57 38

Ketamine in a dose of 100 mg/kg (IP) produced stereotypic behavior and vigorous rotation in adult male Sprague-Dawley rats. The first rotation phase, accompanied by head swinging, was short and terminated by the anesthetic phase which lasted 20-30 min. The second rotation phase began 1-3 min after the end of the anesthetic phase. A single dose of GABA-T inhibitors, gamma-vinyl GABA (1200 mg/kg, IP) or gamma-acetylenic GABA (100 mg/kg, IP) administered 4 hours prior to ketamine, shortened the first rotation phase, increased the anesthetic phase, changed the pattern of postanesthetic rotation and reduced total and net rotation scores. Picrotoxin (3 mg/kg) given 10 min prior to ketamine tended to act in the opposite direction although none of its effects reached statistical significance.
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PMID:Ketamine-induced rotation: interaction with GABA-transaminase inhibitors and picrotoxin. 57 19

A synaptic vesicle fraction was prepared from calf brain cortex, containing 10 identified amino acids and two unidentified ninhydrin-positive compounds, one of which is apparently a peptide. The most plentiful amino acids were taurine (1.8 nmol/g original tissue), glutamic acid (1.8), serine (0.9), aspartic acid (0.8) and GABA (0.8); the others identified were cysteic acid (or cysteinesulphinic acid), glutamine, alanine, glycine and lysine. The unknown peptide occurred in a high concentration (about 16 alanine equivalents/g), and contained mainly aspartic acid and serine. Cysteic acid (or cysteinesulphinic acid) also occurred in relatively high amounts, but its peak contained acid-labile impurities. The influx of [14C]glutamate into the vesicles took place by means of non-saturable migration, while two saturable systems having very similar properties were dominant only at low glutamate concentrations. Influx constants for these quantitatively low uptake systems were Km, 34 and 92 micrometer, and Vmax, 33 and 49 nmol/min/g obtained by v versus v/S plot. Almost the same values were also obtained by a 1/v versus 1/S plot. GAD and GABA-T activities in the vesicles were only 1/200th of those in the synaptosomes.
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PMID:Amino acids in the synaptic vesicle fraction from calf brain: content, uptake and metabolism. 58 77

The effects were examined of two inhibitors of GABA-aminotransferase, amino-oxyacetic acid (AOAA) and RMI-71645-16, on depolarization-induced (30 mM K+) dopamine (DA) release from rat striatal slices. When added to the medium, these drugs increased the release of radiolabeled DA, either accumulated by high-affinity uptake or synthesized from 14C-tyrosine. AOAA did not modify the release of 14C-acetylcholine from striatal slices or 3H-noradrenaline from cortical slices. Moreover, 3H-DA release from substantia nigra was not affected. The data suggest the possibility that the effects of GABA-T inhibitors on striatal DA release are mediated by intrinsic GABA-ergic neurons.
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PMID:Increased dopamine release from rat striatal slices by inhibitors of GABA-aminotransferase. 59 Mar 29

4-Aminobutyrate:2-oxoglutarate (4-aminobutyrate:2-oxoglutarate amino-transferase, EC 2.6.1.19) from human brain has been purified 2500-fold with respect to the initial homogenate. The enzyme, which appears to be pure by polyacrylamide gel electrophoresis, N-terminal analysis and immunodiffusion, was compared to rat brain 4-aminobutyrate transaminase, purified to the same extent in an earlier study [15]. The two enzymes, which have approximately the same molecular weight, show large differences in their tryptic fingerprints and in the peptides produced by cyanogen bromide cleavage. The Km values (limit) for 4-aminobutyrate are different, the human enzyme having four times greater affinity for this substrate. A series of branched-chain fatty acids (including n-dipropylacetate), which are structural analogues of 4-aminobutyrate and inhibit rat brain 4-aminobutyrate transaminase, are less powerful inhibitors of the human enzyme.
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PMID:Comparison of the structural characteristics of the 4-aminobutyrate:2-oxoglutarate transaminases from rat and human brain, and of their affinities for certain inhibitors. 62 69


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