Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.19 (GABA transaminase)
808 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

gamma-Aminobutyric acid transaminase (GABA-Tase; 4-aminobutyrate:2-oxaglutarate aminotransferase, EC 2.6.1.19) immunoreactivity in the rat's cerebellum was studied by light and electron microscopy with indirect immunofluorescence and peroxidase-antiperoxidase methods. Evidence is presented for neuronal and neuroglial compartments of GABA-Tase. Labeled neurons included stellate, basket, Purkinje, and Golgi cells of the cortex and a few large neurons in the deep nuclei. Labeled neuroglia included those surrounding Purkinje cells, their radial fibers in the molecular layer, and astrocytes in the granular layer and deep nuclei. No evidence for sagittal microzonation was found. At the ultrastructural level, GABA-Tase immunoreactive sites were localized to cell surface membranes, intracellular organelles, and the cytoplasmic matrix. GABA-Tase immunoreactivity at synapses could be localized precisely to pre- and postsynaptic membranes in gamma-aminobutyric acid (GABA)-containing as well as non-GABA-containing neurons. Specific label was absent from tissues treated with normal rabbit preimmune sera. GABA-Tase labeling was more intense in tissues from animals anesthetized with ether than with barbiturates and after formaldehyde fixation without glutaraldehyde. Increased GABA-Tase immunoreactivity was observed on treatment with colchicine, GABA with oxamic acid, GABA, harmaline, norepinephrine and glutamate, or diazepam (in order of decreasing effectiveness). Serotonin produced no detectable change, and apomorphine and muscimol decreased the immunoreactivity.
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PMID:Immunocytochemical localization of gamma-aminobutyric acid transaminase at cellular and ultrastructural levels. 28 44

A decrease in brain GABA concentration has been implied as the cause of convulsions induced by hyperbaric oxygen (HOP). We therefore examined the influence of sodium valproate, an anticonvulsant and GABA transaminase inhibitor on HOP-induced convulsions in rats. The mean latency of occurrence of the first electrical discharge in the ECoG and the appearance of the first clinical seizure in awake chronically implanted rats was unchanged by administration of sodium valproate prior to HOP exposure. We conclude that either the sodium valproate inhibition of GABA removal is insufficient to compensate for HOP inhibition of its production, or else that GABA concentration changes are not causally related to HOP-induced seizures.
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PMID:Influence of a GABA transaminase inhibitor on central nervous system oxygen toxicity. 35 31

A detailed presentation of 15 case-histories of subjects of both sexes, drawn from all decennies of life from the first to the eight, suggesting a syndrome originated from a possible GABA deficiency, is carefully made. Such syndrome is believed to be characterized by basic depressive state, loss of the habit of stretching oneself, sleep disorders, mostly with early morning awakening, constipation and nuchal headache. The above symptoms have been associated to a deficiency of GABA after noting the very speed recovery after administration of N-dipropylacetic acid, an inhibitor of GABA transaminase.
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PMID:A syndrome from a possible GABA deficiency. Clinical-therapeutic report on 15 cases. 35 28

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

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

Gabaculine, a specific inhibitor of GABA transaminase, was injected bilaterally into the substantia nigra of rats. One day after injection, GABA was increased 11-fold in the nigra, 6-fold in thalamus and pons-medulla, and 2-fold in pallidum. 5 h after operation, rats showed continuous sniffing and head movement. This behaviour was blocked by a small dose of picrotoxin injected bilaterally into the nigra, but haloperidol (i.p.) was less effective. One day after injection, rats showed high ambulation and this ambulation was blocked by high doses of picrotoxin. On the second day, GABA contents in all regions were less than twice the control level and behaviour had returned to normal. Rats with gabaculine injected into the pallidum or medulla did not show changes of behaviour as seen in rats with injections into the substantia nigra at any of the times. Striatum dopamine turnover was slightly but significantly decreased at 5 h but not at 24 h after intra-nigral injection with gabaculine. The results suggest that gabaculine-induced sniffing and head movement were mediated by nigral GABAergic synapses and were independent of any dopaminergic system, and that the high ambulation at 24 h after operation may have been due to a non-specific effect of abnormal GABA elevation in thalamus and/or nigra.
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PMID:The effects of elevating gamma-amino butyrate content in the substantia nigra on the behaviour of rats. 68 78

The RMI, an irreversible inhibitor of GABA transaminase, inhibited, at the dose of 100 mg/kg, the activity of Mice placed in an open-field. At lower doses, RMI improved the activity in open-field and the number of conditioned avoidance reactions. Results are correlated with increase of the level of brain GABA, following administration of RMI.
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PMID:[Effect of an irreversible inhibitor (RMI71645) of gamma-aminobutyric acid (GABA) transaminase on spontaneous and conditioned activities of mice]. 82 60

1. The activities of the transmitter enzymes acetylcholine esterase (AChE), monoamine oxidase (MAO) and gamma-aminobutyrate transaminase (GABA-TR) were investigated in the nucleus nervi oculomotorii of Salmo irideus (Teleostei) during biomorphosis. 2. AChE as well as MAO-activity could be demonstrated already before the time of hatching, whereas GABA-TR occured from the 10th day post hatching. 3. In earliest stages the AChE activity was found in the neuronal pericarya of the nucleus n. III, but later on a strong increase occured in vestibular presynaptic terminals establishing synaptic contacts with the lateral surface of the large pericarya, especially in the medial part of the dorsal subnucleus and the ventral subnucleus. In adults the enzyme activity was localized in vestibular nerve fiber terminals exclusively due to the loss of enzyme activity in the pericarya. 4. The activity of MAO was found surrounding the neurons of the nucleus nervi oculomotorii with stronger deposits of reaction product at the medial surface that is not occupied by cholinergic terminals. 5. Besides non reacting neurons in all parts of the nucleus some cells in the transition zone between the medial and lateral area of the dorsal subnucleus, exhibited high cytoplasmatic GABA-TR activity. 6. The different ways of chemical transmission between nerve terminals and the neurons of the nucleus nervi oculomotorii are discussed.
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PMID:[Enzyme histochemical investigations of the nucleus nervi oculomotorii of Salmo irideus (Gibbons 1855) during biomorphosis. I. Transmitter enzymes]. 89 18

Two clinically effective anticonvulsants, phenobarbitone and diazepam, protected 5-day old chicks against picrotoxin convulsions without reducing brain GABA-transaminase activity or raising brain GABA concentration. Ethanolamine-O-sulphate and amino-oxyacetic acid, in doses which inhibited GABA-transminase by at least 63% and approximately doubled brain GABA concentration, did not significantly affect the ED50 for picrotoxin convulsions. The ED50 for picrotoxin convulsions was significantly raised by di-n-propylacetate (800 mg/kg) which inhibited GABA transaminase activity by 6% and elevated brain GABA concentration by 26%.
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PMID:Picrotoxin convulsions and GABA metabolism after injection of anticonvulsants in chicks. 99 20

The regional distribution of 9 amino acids, including glutamate and GABA and their metabolising enzymes, has been determined in 5 regions of the frog CNS. Glycine was relatively concentrated in the spinal cord whereas the highest concentration of each of the other amino acids was found in the midbrain. There was a good correlation between the activity of l-glutamate-1-carboxylase (GAD) and the level of GABA in all regions examined and both were concentrated in the midbrain. There was little regional variation in the distribution of 4-aminobutyrate-2-oxoglutarate transaminase (GABA-T).
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PMID:Glutamic acid, GABA and their metabolising enzymes in the frog central nervous system. 107 86


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