Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.15 (glutamate decarboxylase)
 2,169 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The comparative effects of a 10 day estrogen treatment and estrogen independent hyperprolactinemia on nigral and striatal glutamic acid decarboxylase (GAD, EC 4.1.1.15) activity were investigated in male rats. Data obtained show that estrogen treatment decreases GAD activity in substantia nigra, while an increase was observed in conditions of hyperprolactinemia induced by adenohypophysis homograft or acute and chronic sulpiride injection. The possibility of an opposite modulation of strio-nigral GABAergic system by estrogens and prolactin is suggested.
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PMID:Comparative effects of estrogens and prolactin on nigral and striatal GAD activity. 705 6

The AA. have investigated the effects of acute or chronic injection of typical and atypical antidepressants on the activity of the GABA--synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) in discrete brain regions. Very significant changes in GAD activity were only observed with sulpiride and nomifensine, two atypical antidepressants that selectively influence dopaminergic transmission and, in turn, prolactin secretion.
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PMID:Effects of some typical and atypical antidepressants on GAD activity in various brain regions. 709 72

We have investigated the effects of estrogens and prolactin on nigro-striatal dopaminergic function. In this regard, apomorphine-induced hyperactivity has been evaluated in hyperprolactinemic rats. Results obtained suggest the possibility that hyperprolactinemia potentiates nigro-striatal dopaminergic transmission inducing, in chronic, charges in dopamine receptor sensitivity. As a neurochemical parameter of the extrapyramidal motor system, we have investigated the activity of the GABA-synthesizing enzyme glutamate decarboxylase (GAD, EC 4.1.1.15) in corpus striatum and substantia nigra. Hyperprolactinemia induced by anterior pituitary homograft under the kidney capsule or systemic sulpiride injection significantly increases GAD activity. In contrast, estrogen treatment decreases nigral GAD activity even though increases plasma prolactin levels. From a clinical point of view, preliminary data indicating a good therapeutical efficacy of estrogens and progesterone in psychiatric patients are reported.
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PMID:[Modification of the nigro-striatal system by estrogens and prolactin. Clinical and experimental data]. 713 74

The effects of cefazolin, given into the III cerebral ventricle at different doses were studied on GABA content, GAD and GABA-T in the brain-stem of young chickens (Gallus domesticus). A dose-dependent fall in GABA content was observed; GABA decrease was evident 15 min after the administration, reached its nadir at 60 min and disappeared at 120 minutes. Glutamate decarboxylase and GABA-transaminase activity were not significantly changed. Present experiments suggest the excitatory and convulsant effects of cefazolin in chicks are related to GABA depletion in the brain-stem.
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PMID:GABA depletion in chick brain-stem after intraventricular injection of cefazolin. 722 Nov 79

The activity of gamma-aminobutyric acid (GABA) synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) was assayed in the rat substantia nigra (SN) and medial basal hypothalamus (MBH) following systemic injection of different doses of the dopamine receptor agonist apomorphine. In SN, the highest dose of apomorphine (1000 micrograms/kg) causes an increase of the GAD activity whilst an opposite effect is observed with the lowest dose (35 micrograms/kg). Results obtained in SN are in accordance with previous neurochemical and behavioural data suggesting an opposite action of high (500 micrograms/kg) and low doses (100 micrograms/kg) of apomorphine in nigro-striatal system, probably due to the existence of two classes of dopamine receptors, i.e. classical postsynaptic dopamine receptors and presynaptic inhibitory dopamine autoreceptors. In MBH, the evidence for similar effects of low and high doses of apomorphine (the decrease of GAD activity) may suggest that, as already reported, at this level only one class of dopamine receptors is present.
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PMID:[Effects of different doses of apomorphine on the glutamate decarboxylase activity of the substantia nigra and the medial basal hypothalamus]. 731 1

The effects of different doses of the dopamine (DA) receptor agonist apomorphine on the activity of the gamma-aminobutyric acid (GABA)-synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) were investigated in rat substantia nigra in comparison with haloperidol and sulpiride, two DA receptor blocking agents. Results obtained show that low doses (10,35 microgram/kg, s.c.) of apomorphine induce a decrease in nigral GAD activity whilst an opposite effect is observed with the highest dose (1000 microgram/kg, s.c.). No significant change is observed following injection of the intermediate doses (100 and 500 microgram/kg, s.c.). Moreover, sulpiride at the dose used (2 mg/kg, i.p.) induces an increase in GAD activity whilst no effect follows systemic injection of the same dose of haloperidol. The results are discussed in light of recent neurochemical and behavioral data.
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PMID:Effects of different doses of apomorphine on GAD activity in rat substantia nigra. 734 53

The accumulation of GABA in the cerebellum and medulla oblongata-pons of rats has been studied after inhibition of GABA-T (EC 2.6.1.19) by different doses of AOAA. It was found that intraperitoneal (i.p.) injections of AOAA were, at least during the first hour after injection, much less effective than intravenous (i.v.) injections probably due to poor absorption i.p. After i.v. injection, AOAA caused a maximal accumulation of GABA in the cerebellum at a dose of 50 mg/kg. This maximal effect was virtually unchanged up to a dose of 150 mg/kg (the highest dose tested i.v.). If GAD (EC 4.1.1.15) was inhibited by 3-mercaptopropionic acid 30 min after AOAA (90 mg/kg i.v.) the GABA level was stable for at least another 30 min. The rate of GABA accumulation in the cerebellum during the first 15 min after AOAA (50-150 mg/kg i.v.) was 0.086 mumol/g/min and thereafter 0.034 mumol/g/min. It is concluded that AOAA in vivo in a wide dose range inhibits GABA-T almost 100% without affecting GAD to any great extent, and that the onset of action is rapid after i.v. but not after i.p. injection.
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PMID:Effect of aminooxyacetic acid (AOAA) on GABA levels in some parts of the rat brain. 739 47

Charles River CD male rats were randomly divided into 3 groups of five each and placed on folate deficient, folate excess, and control diets respectively. glutamate decarboxylase GAD gamma-amino-butyrate aminotransferase (GABA-T), choline acetltransferase (ChAc), and acetylcholinesterase (AChE) were assayed in the rat brains after 6 weeks of dietary treatment. Neither folate deficiency nor folate supplementation influenced the enzymes associated with GABA and acetylcholine metabolism.
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PMID:Dietary folic acid and the activity of brain cholinergic and gamma-aminobutyric acid (GABA) enzymes. 740 19

The olfactory bulbs in the CNS contain reciprocal dendrodendritic synapses between the granule cells and the secondary dendrites of mitral cells. Based on pharmacologic and electrophysiologic evidence, these synapses are believed to utilize GABA as an inhibitory neurotransmitter. A dendrodendritic synaptosomal fraction has been isolated from rat olfactory bulbs. The upper portion (PB) of the crude nuclear pellet contains 30-40% of the GAD (glutamate decarboxylase) activity of the olfactory bulb homogenate. When PB is purified on a discontinuous sucrose density gradient, 78-85% of the GAD activity is localized to the region containing the dendrodendritic synaptosomes, which were identified by transmission electron microscopy. The presence of a substantial proportion of GAD, the enzyme that catalyzes synthesis of GABA, in the DDS provides neurochemical support for the hypothesis that GABA functions at the reciprocal dendrodendritic synapses in the olfactory bulb.
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PMID:Subcellular distribution of glutamate decarboxylase in rat olfactory bulb: high content in dendrodendritic synaptosomes. 745 75


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