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)

Histochemical and biochemical studies demonstrate that gamma-aminobutyric acid (GABA), glutamic acid decarboxylase (EC 4.1.1.15), and GABA aminotransferase (EC 2.6.1.19) are present in bovine adrenal chromaffin cells. Moreover, [3H]GABA can be taken up and stored by primary cultures of adrenal chromaffin cells. Nicotinic receptor stimulation or KCl depolarization releases the [3H]GABA taken up by these cell cultures. GABA and benzodiazepine recognition sites located in chromaffin cells interact with each other with modalities similar to those described for GABA and benzodiazepine recognition sites located in synaptic membranes prepared from brain tissue. Bicuculline facilitates the release of catecholamine from chromaffin cells induced by nicotinic receptor stimulation but it fails to influence the release of catecholamine evoked by K+ depolarization. Since the GABA-benzodiazepine receptor system appears to modulate nicotinic receptor function, it is suggested that GABA transmission might participate in modulating responsiveness of chromaffin cells to incoming cholinergic stimuli.
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PMID:Intrinsic GABAergic system of adrenal chromaffin cells. 632 6

The distributions of glutamate decarboxylase (EC 4.1.1.15), gamma-aminobutyric acid transaminase (EC 2.6.1.19), and succinate semialdehyde dehydrogenase (EC 1.2.1.24) were determined in monkey retina. The decarboxylase was almost restricted to the inner plexiform layer. The transaminase was also highest in this layer, but activities were 40% as high in the adjacent third of the inner nuclear layer and in the ganglion cell and fiber layers. Succinate semialdehyde dehydrogenase was distributed very differently. Although it also showed a peak of activity in the inner plexiform layer, there was a second equal peak in the photoreceptor inner segment layer and a smaller peak in the outer plexiform layer, regions where both gamma-aminobutyric acid transaminase and glutamate decarboxylase were essentially absent.
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PMID:Distribution of three enzymes of gamma-aminobutyric acid metabolism in monkey retina. 670 30

The distributions of glycine, gamma-aminobutyric acid (GABA), glutamate decarboxylase (EC 4.1.1.15), and GABA transaminase (EC 2.6.1.19) were determined in rabbit and mudpuppy retinas. In both species, peak levels of the amino acids and the enzymes occurred in the inner plexiform layer. Glutamate decarboxylase was almost entirely confined to the inner plexiform layer. Determinations were also made of the GABA content of 107 individual putative amacrine cell somas from mudpuppy retina. About 30% of those somas were found to have high endogenous GABA levels.
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PMID:Distribution of glycine, gamma-aminobutyric acid, glutamate decarboxylase, and gamma-aminobutyric acid transaminase in rabbit and mudpuppy retinas. 670 31

Putative GABAergic neurons in the outer retina of the Texas channel catfish, Ictalurus punctatus, were studied using autoradiographic, biochemical and electrophysiological techniques. A red cone horizontal cell was found to accumulate exogenous GABA in the presence of red light. GABA could be released from these cells with high K+ Ringers solution. The release was only partially blocked by Co2+ and therefore may be only partially Ca2+ dependent. The red cone horizontal cells were found to contain significant activities of L-glutamic acid decarboxylase and GABA transaminase, the enzymes responsible for GABA synthesis and degradation respectively. These data suggest that catfish red cone horizontal cells are GABAergic. To substantiate this, recordings were made from photoreceptors and horizontal cells during the superfusion of the GABA blocking agents bicuculline methochloride or picrotoxin. These agents modified the cone responses in the manner specified if they were blocking the feedback pathway from horizontal cells to cones. Thus it is likely that the horizontal cells are using GABA as the transmitter in the feedback pathway. In addition, the GABA blocking agents were found to interfere with changes in horizontal cell responses which occur during light adaptation.
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PMID:The identification and some functions of GABAergic neurons in the distal catfish retina. 674 Sep 69

The effects of intraperitoneal administration of (S)-4-amino-5-fluoropentanoic acid, a mechanism-based covalent inactivator of gamma-aminobutyric acid transaminase (GABA-T), on whole brain GABA metabolism in mice were investigated. A dose-dependent and time-dependent irreversible inactivation of GABA-T was observed with a concomitant increase in whole brain GABA levels. The compound exhibited no in vitro nor in vivo time-dependent inhibition of glutamate decarboxylase (GAD), alanine transaminase, or aspartate transaminase (Asp-T). It was, however, a potent competitive reversible inhibitor of GAD and a weak competitive inhibitor of Asp-T. The chloro analogue, (S)-4-amino-5-chloropentanoic acid, was ineffective.
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PMID:In vitro and in vivo effects on brain GABA metabolism of (S)-4-amino-5-fluoropentanoic acid, a mechanism-based inactivator of gamma-aminobutyric acid transaminase. 685 67

The neuronal distribution of gamma-aminobutyric acid (GABA) transaminase (GABA-T), the enzyme which metabolizes GABA, has been mapped in rat brain. The method involves staining for newly synthesized GABA-T by the previously established nitro blue tetrazolium technique in animals killed 8-48 hours after administration of gabaculine, an irreversible inhibitor of GABA-T. Neuronal staining is obscured by staining of other elements if initial suppression is inadequate or survival times postgabaculine are too long. With appropriate conditions, GABA-T-positive neuronal somata can be widely detected. The stained cells include neuronal groups previously reported to be GABAergic on the basis of glutamate decarboxylase (GAD)-colchicine immunocytochemistry and other methods, i.e.: Purkinje, basket, Golgi, and stellate neurons of the cerebellum; basket and stellate neurons of the hippocampus; granule and periglomerular cells of the olfactory bulb; magnocellular neurons of the hypothalamus; and neurons of the striatum, pallidum, entopeduncular nucleus, cortex, medial septal area, diagonal band, substantia innominata, reticular nucleus of the thalamus, substantia nigra, and dorsal raphe. Other cells that stain intensely for GABA-T and may be GABAergic include neurons in the midlateral septal area, accumbens, the central medial and basal nuclei of the amygdala, zona incerta, the brainstem reticular formation, central gray, interstitial nucleus of Cajal, and various thalamic nuclei including the periventricular, intralaminar, rhomboid, and subparafascicular. Known non-GABA neuronal groups are negative for GABA-T staining under these conditions, reinforcing the hypothesis that GABA neurons are far more GABA-T intensive than other neurons.
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PMID:Distribution of GABA-T-intensive neurons in the rat forebrain and midbrain. 688 73

Effect of short light and dark adaptations on retinal GABA and taurine was studied using bull frog (Rana catesbiana). The retinal GABA was increased significantly in light-adapted state, and this increase was accompanied by the increases of L-glutamate decarboxylase (GAD) activity and [3H]-GABA release. The activation of retinal GABA-transaminase succinic semialdehyde dehydrogenase (GABA-T:SSADH) was also observed after a lag period of several hours. Under the same experimental conditions, however, no significant changes were noted in retinal taurine content and cysteine sulfinate decarboxylase (CSD) activity. These findings suggest that a short light adaptation induces differential effects on retinal GABA and taurine, and the activation of GABAergic neurons in the retina may be involved in the process of short light adaptation.
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PMID:Alteration of GABA system in frog retina following short light and dark adaptations - a quantitative comparison with retinal taurine. 697 82

Alteration of metabolism of taurine in prolonged light- and dark-adapted frog retinae were studied in comparison with that of gamma-aminobutyric acid (GABA) and the following results were obtained. (1) Statistically significant alterations in retinal taurine, an increase in dark-adapted, and a decrease in light-adapted states, respectively, occurred when frogs were adapted continuously to light or dark for more than 3 weeks. Under the same experimental conditions, no alteration in retinal GABA was noted. (2) At 3 weeks and thereafter, a significant increase of retinal cysteine sulfinic acid decarboxylase (CSD; EC 4.1.1.12) activity, an enzyme involved in the biosynthetic pathway of taurine, also occurred in the dark, whereas the activity in the light-adapted retina was reduced. On the other hand, the retinal activity of L-glutamate decarboxylase (GAD; EC 1.1.1.15), the rate-limiting enzyme of GABA biosynthesis, was not altered in dark- as well as light-adapted state. Similarly, retinal GABA-transaminase (GABA-T; EC 2.6.1.19)-succinic semialdehyde dehydrogenase (SSADH; EC 1.2.1.16) was unaltered. (3) These alterations in retinal taurine were, however, unaccompanied by any changes in factors related to transmitter actions such as evoked release, high affinity uptake, and specific binding to synaptic membranes. The above results suggest that, different from GABA as a potent candidate for inhibitory neurotransmitter, retinal taurine may act as neuromodulator and/or may play an important role as a basic factor for maintaining cellular integrity under certain pathophysiological conditions.
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PMID:Alteration of metabolism of retinal taurine following prolonged light and dark adaptation: a quantitative comparison with gamma-aminobutyric acid (GABA). 697 81

Ethanolamine O-sulphate (EOS) dissolved in the drinking water (5 mg . ml(-1) was administered ad libitum to rats for 26 days. At the end of this period, glutamate decarboxylase (GAD) and GAA-transaminase (GABA-T) activities, 4-aminobutyrate (GABA) concentration, and the levels of six other amino acids were measured in various brain regions. Significant inhibition of GABA-T accompanied by significant increases in GABA content were observed throughout the brain, although the magnitudes of these effects varied according to region. GAD activity was significantly reduced in most brain regions, although this effect was apparently not related to cofactor availability or the direct actions of EOS or increased GABA concentration. Glutamine levels were significantly reduced to approximately 72% of control values in all brain regions. Aspartate levels were significantly reduced to approximately 84% of control values in all regions except the striatum and cerebellum. Minor changes in other amino acid levels were also detected. These neurochemical changes which accompanied the primary effect of EOS on GABA-T are discussed in terms of indirect secondary metabolic changes rather than nonspecific enzyme inhibition by EOS.
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PMID:A regional study of 4-aminobutyrate metabolism and amino acid levels in rat brain following chronic oral administration of ethanolamine O-sulphate. 706 27

The effects of gamma-aminobutyric acid (GABA)-alpha-oxoglutarate aminotransferase (GABA-T) inhibitors, L-glutamic acid decarboxylase (GAD) inhibitors, and antipetit mal anticonvulsants on gamma-hydroxybutyric acid (GHB) and GABA were studied. Treatment with anticonvulsants and GABA-T inhibitors resulted in an increase in steady-state brain levels of both GHB and GABA. GAD inhibitors produced markedly decreased levels of brain GABA but no change in GHB concentrations. Studies of GHB derived exclusively from GABA showed that GABA-T inhibitors which produced an elevation of steady-state levels of GHB in brain also resulted in a decrease in GABA-derived GHB. Intracerebroventricular (i.c.v.) administration of GABA, putrescine, and 1,4-butanediol all produced significant elevations in brain GHB, but GABA-T inhibitors blocked this effect of GABA and putrescine. These data suggest that there may be another source for GHB in brain in addition to GABA and raise the possibility that 1,4-butanediol may be that source.
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PMID:Studies on the relation of gamma-hydroxybutyric acid (GHB) to gamma-aminobutyric acid (GABA). Evidence that GABA is not the sole source for GHB in rat brain. 715 69


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