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)

The GABA system was studied in different regions of the rat's brain following inhibition of brain GABA catabolism with intracisternal ethanolamine-O-sulphate or intraperitoneal aminooxyacetic acid. Both treatments lowered GABA aminotransferase and glutamate decarboxylase activities to similar extents in equivalent nuclei on either side of the brain. However, GABA contents were elevates to a consistently higher level in the right-hand substantia nigra, superior colliculus and nucleus accumbens, and in the left-hand ventral tegmentum, ventromedial thalamus and caudate nucleus, with no bilateral asymmetry evident in globus pallidus. These findings are discussed with reference to possible inherent inequalities in the functional states similar GABA systems on opposite sides of the brain.
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PMID:Bilateral asymmetry in brain GABA function? 727 13

Mice infected with the Venezuelan equine encephalomyelitis virus showed a significant decrease in the GABA content of cerebral hemispheres. Activity of the enzyme which synthetizes GABA, glutamate decarboxylase, is also reduced in whole cerebral hemispheres, neostriatum, and frontal cortex of infected animals, as compared to values obtained from the same regions of control mice. No significant difference was demonstrated in the activities of GABA transaminase, glutamate dehydrogenase, lactate dehydrogenase, succinate dehydrogenase and NAD-malate dehydrogenase in any of the regions studied. The results suggest that the viral infection produced an alteration in the mechanism of GABA synthesis.
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PMID:GABA metabolism in Venezuelan equine encephalomyelitis virus infection. 736

The porphyrin precursor delta-aminolevulinic acid (delta-ALA) is a structural analogue of the putative amino acid neurotransmitter, gamma-aminobutyric acid (GABA). This study has demonstrated that delta-ALA has no effect on glutamate decarboxylase activity and only a small inhibitory effect of GABA aminotransferase activity. This would suggest that if accumulation of delta-ALA is related to development of the acute attack of porphyria, it is not via an effect on GABA synthesis and metabolism.
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PMID:The effect of delta-aminolevulinic acid on the synthesis and metabolism of GABA in rabbit brain homogenates. 736 97

To obtain more insight into the physiological role of gamma-aminobutyric acid (GABA) in rat salivary glands, we measured the concentration of GABA and the activities of its biosynthetic and metabolic enzymes, glutamate decarboxylase (GAD) and GABA transaminase (GABA-T). The GABA concentrations in rat parotid and submandibular glands were 10.0 and 14.3 nmol/g weight, respectively, which were 0.6-0.8% of the levels in the brain (cerebellum and medulla oblongata), whereas glutamic acid (Glu) was abundant in the two glands. These GABA levels in the two glands were significantly decreased by administration of semicarbazide (200 mg/kg, i.p.), a GAD inhibitor, and increased by gabaculine (50 mg/kg, i.p.), a GABA-T inhibitor. The activities of both GAD and GABA-T were also detected in homogenates of the two salivary glands, but they were lower than those in the brain. However, kinetic analysis showed that the values of Michaelis constants for Glu and GABA in both enzyme reactions in these two glands were similar to those in the brain. These results indicate that GABA and its biosynthetic and metabolic enzymes are present in rat salivary glands as well as the brain.
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PMID:Existence of gamma-aminobutyric acid and its biosynthetic and metabolic enzymes in rat salivary glands. 765 Aug 68

The C57BL/10 SPS/sps mouse mutant are audiogenic seizure-susceptible. The enzymatic activities of glutamate decarboxylase (GAD), GABA aminotransferase (GABA-T), alanine aminotransferase (ALA-T), aspartate aminotransferase (ASP-T), and glutamate dehydrogenase (GDH) of whole brain supernatant are significantly reduced in these epileptic mice. GABA uptake is decreased in cortex, midbrain, and pons medulla. Previous studies showed the presence of two sodium-dependent GLU uptake systems in normal (SPS/SP) mice. Glutamate Umax by System 1 is significantly decreased in these mice, whereas the Umax value for System 2 is significantly increased in the epileptic mice.
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PMID:Altered GABAergic and glutamatergic transmission in audiogenic seizure-susceptible mice. 788 3

1. The modulatory effects of L-glutamate and its structural analogues, and of gamma-aminobutyric acid (GABA), on sympathetic co-transmission were studied in the rat isolated vas deferens exposed to electrical field stimulation (EFS). 2. Application of exogenous L-glutamate caused a concentration-dependent (1 microM-3 mM) inhibition of the rapid twitch component of the biphasic EFS contraction. However, L-glutamate (1 microM-3 mM) had a minimal effect on the phasic contraction induced by exogenous adenosine 5'-triphosphate (ATP, 150 microM) and noradrenaline (50 microM). Unlike L-glutamate, D-glutamate had no effect on the EFS contraction. 3. The L-glutamate-induced inhibition of the EFS contractions was significantly attenuated by the glutamate decarboxylase (GAD) inhibitor 3-mercapto-propionic acid (150 microM) and was abolished in the presence of the GABA transaminase (GABA-T) inhibitor, 2-aminoethyl hydrogen sulphate (500 microM). 4. The L-glutamate-induced inhibition of the electrically evoked contraction was not affected by the adenosine A1-receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX)(30 nM), reactive blue 2 (30 microM) or the GABAA receptor antagonist bicuculline (50 microM). However, the GABAB receptor antagonist 2-hydroxysaclofen (50 microM) significantly inhibited the L-glutamate effect. 5. Similar to L-glutamate, GABA also caused a concentration-dependent (0.1-100 microM) inhibition of the EFS contractions. This GABA-induced inhibition was not affected by either the GABAA receptor antagonist bicuculline (50 microM) or reactive blue 2 (30 microM). However, a significant attenuation of the GABA-mediated effect was recorded with the GABAB receptor antagonist 2-hydroxysaclofen (50 microM). Contractions of the vas deferens induced by exogenous ATP and noradrenaline were not affected by GABA (0.1-100 microM). 6. The L-glutamate analogues, N-methyl-D-aspartate (NMDA) (1 microM-1 mM) and quisqualate (Quis 0.1 microM-0.3 mM) had no effect, whilst kainate (Kain, 1 microM-1 mM) caused an inhibition of the EFS-induced contractions. Effects of Kain could be abolished by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dioxine (CNQX, 10 microM). NMDA, Quis and Kain had no effect on the exogenous ATP- or noradrenaline-induced contractions. 7. It is concluded that the excitatory amino acid L-glutamate modulates the electrically evoked vas deferens contraction through conversion to the inhibitory amino acid GABA by a specific GABA transaminase. The GABA formed may then act on GABAB receptors and cause inhibition of the contraction through a presynaptic mechanism.
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PMID:Presynaptic modulation by L-glutamate and GABA of sympathetic co-transmission in rat isolated vas deferens. 876 4

The effects of changes in gamma-aminobutyric acid (GABA) metabolism or inhibitory processes was studied in the perforant path-dentate gyrus synapses in rat cortico-hippocampal slices, and in the monosynaptic-reflex circuit in isolated newborn, rat spinal cord. GABA metabolism was modulated by pharmacological block of either the anabolic enzyme glutamate decarboxylase (GAD) or the catabolic enzyme GABA transaminase (GABA-T). The results support the notion that GABA concentration determines the efficacy of inhibition in these regions of the central nervous system (CNS).
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PMID:GABA metabolism controls inhibition efficacy in the mammalian CNS. 890 31

Previous studies have demonstrated that the expression of one of the isoforms of glutamate decarboxylase, GAD67, is selectively reduced in cultured cortical neurons and in rat cerebral cortex when the concentration of GABA is elevated. We asked whether the expression of GAD67 was similarly affected by elevated GABA throughout the brain. The concentration of GABA in rat brain was increased by inhibiting GABA transaminase (GABA-T) with vigabatrin (gamma-vinylGABA, GVG), an antiepileptic drug and selective inhibitor of GABA-T. Rats were injected with saline or vigabatrin (150 mg/kg) daily for 5 days, and the effects of accumulated GABA on total GAD activity and the expression of GAD65 and GAD67 proteins were determined in twelve brain regions. The GABA concentration was significantly elevated in all regions except amygdala and olfactory bulb after vigabatrin treatment. Total GAD activity was significantly lower than controls in six regions: cerebellum, frontal cortex, thalamus, substantia nigra, ventral tegmentum, and the remaining midbrain. The decrease in GAD activity was largest in cerebellum and thalamus (33% and 29%), while the changes in the other four areas were 15-18%. Vigabatrin treatment significantly reduced GAD67 protein in all regions except olfactory bulb, whereas GAD65 protein decreased significantly only in cerebellum. The failure to detect significant changes in GAD activity in regions having a significant change in GAD67 levels is attributable to the small contribution of GAD67 to total GAD in those regions. It is evident that there are marked regional differences in the effects of tissue GABA levels on the expression of GAD67.
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PMID:Elevation of brain GABA levels with vigabatrin (gamma-vinylGABA) differentially affects GAD65 and GAD67 expression in various regions of rat brain. 966 22

Effects of iron deficiency on the distribution of iron and glutamate decarboxylase (GAD), gamma-aminobutyric acid transaminase (GABA-T) activities and GABA concentrations in different brain regions in young rats were investigated. Iron deficiency was induced by feeding an iron-depleted diet (0.32mg/100g) in weanling rats for 3 weeks or 6 weeks. The values of hemoglobin (Hb), hematocrit (Ht) and red blood cells (RBC) decreased with the progress of anemia. The concentrations of serum iron in the rats fed iron-depleted diets were lower than those of corresponding controls. On the other hand, the concentrations of total iron-binding capacity (TIBC) and unsaturated iron-binding capacity (UIBC) in serum were higher than those of corresponding controls. These results showed that hypochromic and typical iron-deficiency anemia had occurred in these rats. At the same time, iron deficiency also resulted in significantly low iron concentrations in the brain, especially in the hypothalamus, midbrain and thalamus, and striatum and hippocampus. Although the changes in GABA concentrations in corresponding brain regions were not observed, the activities of the GABA-synthesizing enzyme GAD and GABA-degrading enzyme GABA-T of the rats fed iron-depleted diets for 6 weeks decreased significantly. This study provides evidence that iron deficiency in the brain could change the utilization and metabolism of GABA.
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PMID:Effects of iron deficiency on iron distribution and gamma-aminobutyric acid (GABA) metabolism in young rat brain tissues. 971 48

Diabetes mellitus (DM) often causes neural dysfunctions, including visual disorders. To investigate the effect of hyperglycemia on the visual system, we studied the metabolism of gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter that has an important role in visual functions. We determined the GABA content and activities of glutamate decarboxylase (GAD) and GABA transaminase (GABA-T) in the retina and superior colliculus (SC) in streptozotocin (STZ)-induced DM rats. The GABA content and activities of GAD and GABA-T were decreased in the retinas of STZ-treated rats. The GABA content and GAD activity were reduced in the SC of STZ-treated rats, whereas GABA-T activity showed no marked change. This GABA reduction in the diabetes may be correlated with visual dysfunctions.
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PMID:Alteration of the GABAergic neuronal system of the retina and superior colliculus in streptozotocin-induced diabetic rat. 984 53


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