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At least 1,171 records · Page 65Linked to original sources
PubMed1988

Mechanism of inactivation of gamma-aminobutyric acid aminotransferase by (S,E)-4-amino-5-fluoropent-2-enoic acid.

Evidence for an enamine mechanism of inactivation of pig brain gamma-aminobutyric acid (GABA) aminotransferase by (S,E)-4-amino-5-fluoropent-2-enoic acid is presented. apo-GABA aminotransferase reconstituted with [3H]pyridoxal 5'-phosphate is inactivated by (S,E)-4-amino-5-fluoropent-2-enoic acid and the pH is raised to 12. All of the radioactivity is released from the enzyme as an adduct of the cofactor; no [3H]pyridoxamine 5'-phosphate is generated.

4-Aminobutyrate Transaminase↗
PubMed2000

The alteration of gamma-aminobutyric acid and glutamate contents in the discrete brain of female tilapia during certain stages of gonadal cycle.

The alteration of gamma-aminobutyric acid (GABA) and glutamate (Glu) contents in the discrete brain of female tilapia during the certain stages of gonadal cycle was investigated. Both hypothalamic GABA and Glu showed a significantly higher content in the prespawning female than that in the recrudesced and regressed females, which there was no significant difference. In the different gonadal status of female, both telencephalic GABA and Glu showed a maximal content during the prespawning phase and a minimal content during the recrudesced phase. Neither GABA nor Glu content was altered with the gonadal phases in the optic lobe and cerebellum of female tilapia. These results indicate that the alteration of GABA and Glu contents in the hypothalamus and telencephalon, but neither in the optic lobe nor cerebellum, is consistent with the gonadal cycle.

Animals↗
PubMed1981

Differential effects of gamma-aminobutyric acid (GABA)-elevating agents on the neuroleptic-induced activation of striatal tyrosine-hydroxylase: evidence that di-n-propylacetate augments GABAergic neurotransmission.

Di-n-propylacetate (DPA), in contrast to many other agents which elevate brain gamma-aminobutyric acid (GABA) content, appears to increase GABA selectively in a compartment that is associated with nerve terminals. In order to determine whether the DPA-induced increase in nerve-terminal GABA could augment GABAergic transmission in substantia nigra, we examined the ability of DPA to influence nigrostriatal dopamine function. For this purpose, the neuroleptic-induced activation of striatal tyrosine hydroxylase (TH) was selected as a model system. Neuroleptic drugs, such as haloperidol, cause an allosteric activation of striatal TH which can be measured in vitro as a decrease in the Km of TH for cofactor (2-amino-4-hydroxy-6,7-dimethyl-5,6,7,8-tetrahydropterine). This effect can be reversed by treatment with GABA-receptor agonists. We therefore examined the ability of DPA to reverse the activation of striatal TH induced by haloperidol. DPA was able to reverse the haloperidol-induced activation of striatal TH in doses which caused a 30 to 50% increase in GABA in substantia nigra. The action of DPA was completely antagonized by treatment with bicuculline, a GABA-receptor antagonist, indicating that the effect of DPA is mediated via GABA receptors. The effect of amino-oxyacetic acid was also examined, since our previous evidence suggested that the GABA increase after this agent was largely associated with compartments of GABA other than nerve terminals. Amino-oxyacetic acid was less effective than DPA in preventing the haloperidol-induced activation of TH, despite the fact that nigral GABA was increased by 30 to 100%.

Aminooxyacetic Acid↗
PubMed1995

Extracellular gamma-aminobutyric acid in the substantia nigra reticulata measured by microdialysis in awake rats: effects of various stimulants.

The gamma-aminobutyric acid (GABA)-ergic system in the substantia nigra reticulata (SNR) was challenged by local infusion of various receptor-specific agents to obtain additional information on the physiological significance of extracellular GABA levels as measured by microdialysis in awake rats. Notwithstanding in vitro results, basal extracellular GABA levels were not affected by local infusion of the GABA-A agonist muscimol or by infusion of the GABA-B agonist baclofen. Upon a dopaminergic challenge, the D2 agonist LY 171555 was equally ineffective, but the D1 agonist induced an increase in extracellular GABA levels, which persisted in the presence of tetrodotoxin (TTX). Using excitatory amino acids, kainic acid was ineffective in modulating GABA levels, whereas N-methyl-D-aspartate induced an increase in extracellular GABA levels, again persisting when co-infused with TTX. The functional significance of TTX-independent changes in extracellular GABA levels is discussed.

Animals↗
PubMed1982

[Turnover of gamma-aminobutyric acid (GABA) in neurons and glial cells of the chick embryo in culture].

The turnover rates of gamma-aminobutyric acid (GABA) in cultured neurons and glial cells of Chicken embryo were measured by using a gas chromatography/mass spectrometric method. The method followed involved monitoring of the time course of changes in the enrichment of deuterium in GABA following incubation with pentadeuterated glutamate in the medium. The GABA turnover rate in neurons was found to be nearly eight fold greater than in glial cells.

Animals↗
PubMed1977

The effects of gamma-aminobutyric acid on prolactin and gonadotropin secretion in the unanesthetized rat.

The effects of the intraventricular injection of gamma-aminobutyric acid (GABA) on pituitary secretion of luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin (PRL) were examined in Na-pentobarbital (PB)-anesthetized and unanesthetized male rats. GABA (5 or 10 millimicronmol) injected into the lateral ventricle of PB anesthetized rats resulted in significant elevations in plasma concentrations of LH and PRL. When administered via a lateral ventricle cannula to unanesthetized rats, GABA (1, 5, or 10 millimicronmol) caused a significant increase in plasma PRL levels but had no effect on plasm LH concentrations. Plasma FSH was uninfluenced by GABA in all animals studied. The data indicate that PB anesthesia can alter the hypothalamic pituitary axis to a possible neurotransmitter agent.

Aminobutyrates↗
PubMed1984

Relationships of structure to binding of gamma-aminobutyric acid (GABA) and related compounds with the GABA and benzodiazepine receptors.

The relationship of the structure of gamma-aminobutyric acid (GABA) and 45 related compounds to their binding with the GABA and benzodiazepine (BDZ) receptors was investigated. In the course of evaluating the cross-reactivity of the 45 GABA-related compounds in a GABA radioreceptor assay (GABA-RRA) using [3H]GABA and rat brain synaptic membranes, it became clear that for the molecule to react with GABA-receptors the amino group must be free, but that the carboxy group is not essential. It was also demonstrated that the molecule lost its cross-reactivity if the distance between the alpha-carbon and the amino group exceeded a certain limit, and, additionally, that the cross-reacting potency depended on the stereospecificity of the compound. When the cross-reactivity of GABA related compounds with the GABA receptor was compared with their enhancement of BDZ receptor affinity, a parallelism was found between the two actions. Between d-gamma-amino-beta-hydroxybutyric acid (d-GABOB) and 1-GABOB, however, no difference was found in the BDZ receptor affinity-enhancing effect, although there was a large difference in the cross-reactivity in the GABA-RRA. This indicates that the stereospecificity of the beta-carbon is crucial for the binding of the molecule to the GABA receptor but not essential for its binding to the BDZ receptor, suggesting that the GABA receptor and the BDZ receptor each recognize a different site of the molecule.

Animals↗
PubMed1991

Gamma-aminobutyric acid enhancement of potassium-stimulated release of [3H]norepinephrine by multiple mechanisms in rat cortical slices.

Gamma-Aminobutyric acid (GABA) and GABAA agonists enhance stimulated release of [3H]norepinephrine [( 3H]NA) in several regions of the rat brain. In this study, the mechanisms by which GABA and GABAergic agonists augment potassium-stimulated release of [3H]NA from rat frontal cortical slices were examined. GABA enhanced potassium-stimulated [3H]NA release, but did not alter release of [3H]NA evoked by the calcium ionophore A23187, 10(-5) M, either in the presence or the absence of extracellular calcium. The effect of GABA on potassium-stimulated [3H]NA release was apparently reduced by the GABAA antagonist bicuculline methiodide, 10(-4) M, and by the selective inhibitor of GABA uptake SKF 89976A, 10(-5) M, but was abolished only when bicuculline methiodide and SKF 89976A were present in combination. The GABAA agonist muscimol enhanced potassium-stimulated release of [3H]NA in a manner similar to GABA. In addition, nipecotic acid, a substrate for GABA uptake, enhanced potassium-stimulated [3H]NA release. Thus, GABA appears to enhance potassium-stimulated [3H]NA release by acting upon both GABA uptake and GABAA receptors. The GABAA receptors involved in this effect may be a subtype of GABAA receptors since they are not modulated by benzodiazepines. These results support the involvement of the GABA uptake carrier and the GABAA receptor in mediating the enhancement by GABA of potassium-stimulated [3H]NA release in the cortex of the rat.

Animals↗
PubMed1989

Effect of gamma-aminobutyric acid on bombesin-evoked release of somatostatin and gastrin from isolated rat stomach.

The effect of gamma-aminobutyric acid (GABA) on basal and bombesin (BBS)-stimulated release of somatostatin (SLI) and gastrin from isolated perfused rat stomach was examined. In the control study, BBS at a dose of 10 nM significantly stimulated release of SLI and gastrin. Infusion of GABA (1-1000 nM) caused a depression of SLI release induced by BBS (10 nM) in a dose-dependent fashion. However, at doses used in this study GABA had no effect on either basal level of SLI and gastrin or BBS-elicited gastrin release. These results indicate that GABA can specifically modulate BBS-induced SLI release from rat stomach.

Animals↗
PubMed1985

Specific [3H]gamma-aminobutyric acid binding to vestibular membranes of the chick inner ear.

To support a postulated neurotransmitter character of gamma-aminobutyric acid (GABA) in the vertebrate vestibule, [3H]GABA binding was measured in a crude membrane preparation of chick inner ear ampullary cristae. In the absence of divalent cations bound [3H]GABA was displaced by unlabeled GABA, muscimol or bicuculline, but it was not displaced by (+/-)-baclofen. A single population of [3H]GABA binding sites with an equilibrium constant of 19.4 nM and a maximum binding capacity of 0.58 pmol/mg protein was found. These results suggest the possible existence of a synaptic GABAA receptor in the chick inner ear membranes and sustain the neurotransmitter role of GABA in the chick vestibule.

Animals↗
PubMed1990

Effect of gamma aminobutyric acid on the carbon dioxide rebreathing response of normal subjects: a study using vigabatrin.

Animal studies suggest that gamma aminobutyric acid (GABA) may be an important neurotransmitter in the control of respiration. Vigabatrin, a new drug for the treatment of epilepsy, is thought to exert its effect by increasing GABA concentrations in the brain. To assess the effect of increased GABA concentrations in the brain on human respiration we measured the ventilatory response to carbon dioxide in seven normal subjects after they had taken vigabatrin or placebo for three days in a double blind crossover study. There was no change in either the slope or the intercept of the curve of the ventilatory response to carbon dioxide after vigabatrin by comparison with placebo. This study suggests that GABA does not have an important role in the control of respiration in normal individuals.

4-Aminobutyrate Transaminase↗
PubMed1987

Voltage-clamp studies of the inhibition of gamma-aminobutyric acid response by glucocorticoids in bullfrog primary afferent neurons.

Acute effects of glucocorticoids on the response to gamma-aminobutyric acid (GABA) were examined in primary afferent neurons in bullfrog spinal ganglia, using intracellular and voltage-clamp recording techniques. Prednisolone and hydrocortisone (5 microM to 1 mM) caused a dose-dependent decrease in the amplitude of GABA-induced depolarization, while having no effect on the membrane potential and resistance of the neuron. Prednisolone depressed the muscimol-induced depolarization. Nipecotic acid, a blocker of GABA uptake, did not influence the inhibitory action of prednisolone. Voltage-clamp analyses showed that the inward current induced by an iontophoretic application of GABA (GABA current) was suppressed by prednisolone and hydrocortisone. The depression of the GABA current is neither due to a blockage of open channels nor a facilitation of the desensitization of GABA receptors. Prednisolone shifted the dose-response curve of the GABA current downward. The double-reciprocal (Lineweaver-Burk) plot showed that the maximum GABA current was reduced by prednisolone, suggesting a non-competitive antagonism. These results suggest that glucocorticoids suppress the GABA-induced chloride current, decreasing the number of functional channels associated with GABAA receptor.

Afferent Pathways↗
PubMed1982

Inhibitory action of gamma-aminobutyric acid on the excitatory but not inhibitory innervation of the rat anococcygeus muscle.

1 The effects of gamma-aminobutyric acid (GABA), ethylenediamine, 3-aminopropane sulphonic acid and (+/-)-baclofen have been examined on the responses to stimulation of the adrenergic excitatory and non-adrenergic non-cholinergic inhibitory innervation of the rat anococcygeus muscle in vitro. 2 GABA produced a dose-related depression of the contractile responses to field stimulation. Ethylenediamine and baclofen also depressed the contractile responses, though they were less potent than GABA. 3-Aminopropane sulphonic acid was almost inactive. The inhibitory action of GABA was not modified by phentolamine, propranolol or bicuculline methylbromide. 3 GABA did not affect the contractile responses of the anococcygeus muscle to noradrenaline, phenylephrine or carbachol in untreated muscles or those treated with 6-hydroxydopamine in vitro. 4 In preparations in which tone was raised by continuous perfusion with carbachol in the presence of phentolamine, field stimulation relaxed the muscle. GABA had no effect on this inhibitory response, and did not itself produce any relaxation. 5 It is concluded that GABA exerts a presynaptic inhibitory action on the excitatory adrenergic but not on the inhibitory innervation of the anococcygeus muscle, and that the GABA receptor involved exhibits properties of the previously described GABAB site.

Animals↗
PubMed1993

[Relationship between the presynaptic depolarization effect of acupuncture and r-aminobutyric acid, opioid peptide and substance P].

The present study was performed on 22 cats to explore whether r-aminobutyric acid (GABA), endogenous opioid peptide and substance P (SP) were involved in the regulation of presynaptic inhibition in acupuncture analgesia. The size of the antidromic compound C action potentials of the sural nerve evoked by the testing stimulation in spinal cord was measured as an indicator of C-afferent terminal excitability. It was found that the electro-acupuncture (EA) at "Huantiao" (GB30) and "Yang lingquan" (GB34) points induced significant enlargement of the antidromic C-waves, showing the depolarization of presynaptic terminals of primary C-afferents was enhanced. The depolarization effect of EA was significantly reduced by bicuculline, naloxone and the antiserum of SP locally applied to the surface of spinal cord respectively. It is supposed that GABA, endogenous opioid peptide and SP may be involved in the regulation of presynaptic inhibition in acupuncture analgesia.

Action Potentials↗
PubMed1982

Concentration gradients of free and total gamma-aminobutyric acid and homocarnosine in human CSF: comparison of suboccipital and lumbar sampling.

Concentrations of free and total gamma-aminobutyric acid (GABA) and homocarnosine were determined in sequential aliquots of the first 30 ml of CSF obtained by lumbar puncture in five patients. Rostrocaudal gradients were calculated and compared to gradients estimated by determining concentrations of these substances in CSF obtained by simultaneous suboccipital and lumbar punctures in four more patients. In the lumbar fractions study, rostrocaudal mean gradients of 0.36, 36, and 21 pmol/ml for free GABA, total GABA, and homocarnosine, respectively, were calculated. In the suboccipital/lumbar study, gradients of 0.33, 30, and 24 pmol/ml for free GABA, total GABA, and homocarnosine, respectively, were estimated. These results indicate that valid comparison of CSF concentrations of these substances is restricted to similar fractions and suggest that in CSF the substances originate largely from brain rather than from peripheral sources.

Adult↗
PubMed1987

The quantification of gamma-aminobutyric acid in the cerebrospinal fluid by a radioreceptorassay.

The development of a radioreceptor assay designed to measure gamma-aminobutyric acid (GABA) in CSF is described. The method is based on the presence of high affinity and selective GABA binding sites obtained from rat brain membrane preparations treated with 0.05% Triton X-100. The optimum protein concentration in the incubation medium, the duration of incubation to reach equilibrium, the temperature and the optimum pH are discussed. The standard curve permits measurements in the range 35 to 2250 nmol/l GABA. The imprecision of the method calculated from three different concentrations: 1125, 562 and 281 nmol/l shows coefficients of variation for 'within' and 'between' assays, between 5.2% and 9.3% and between 7.4% and 12.4%, respectively. The percentage of recovery is 102 +/- 3.3% (n = 4). This radioreceptorassay has a sensitivity of 14 nmol/l. The method is easy, rapid and not expensive. It enables analysis of small volumes of CSF (200 microliters). Several samples (greater than 20) can be analysed in the same run in about one hour.

Animals↗
PubMed1995

beta-Carboline gamma-aminobutyric acidA receptor inverse agonists modulate gamma-aminobutyric acid via the loreclezole binding site as well as the benzodiazepine site.

The benzodiazepine site on the gamma-aminobutyric acid(A) (GABAA) receptor is the principle site of action for a number of structurally diverse compounds, including the beta-carbolines, many of which bind with high affinity. The apparent reversal of inhibition and potentiation by high concentrations of methyl-6,7-dimethoxy-4-ethyl-beta-carboline (DMCM) and other beta-carbolines has been reported by several groups and is insensitive to the benzodiazepine antagonist Ro 15-1788. By using alpha 6-containing receptors, which have low affinity for benzodiazepines, we observed robust potentiation of GABAA responses by micromolar concentrations of DMCM and other beta-carbolines that is dependent on the beta subunit variant. The beta subunit-dependent potentiation by the anticonvulsant loreclezole is dependent on a single amino acid in the putative transmembrane 2 region. By using single point mutations that discriminate the loreclezole site, we show that potentiation by DMCM is also dependent on the presence of the same amino acid, Asn290, in beta 2 or beta 3 (serine in beta 1), providing evidence that the low affinity site for beta-carboline potentiation is the loreclezole site. The potentiation is independent of the alpha subunit and is more pronounced on alpha 6-containing receptors due to the lack of DMCM inhibition via the benzodiazepine site. In addition, the potentiation observed is competitive with that of loreclezole, and other beta-carbolines, such as ethyl-beta-carboline-3-carboxylate and propyl-beta-carboline-3-carboxylate, act in a similar manner. The finding that beta-carbolines can act via the loreclezole site as well as the benzodiazepine site suggests that a wider variety of compounds may act via this site and shows that compounds can interact with more than one modulatory site on the GABAA receptor.

Animals↗
PubMed1984

Role of the gamma-aminobutyric acid receptor-ionophore complex in seizure disorders.

The possibility of a role for the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in seizure disorders has been strengthened by biochemical studies showing that various nervous system depressant drugs can modulate GABA receptor binding in vitro. In particular, two classes of anticonvulsant agents, the benzodiazepines and the barbiturates, have modulatory receptor sites on the GABA receptor-ionophore protein complex of the postsynaptic membrane. Furthermore, it is well established that direct block of GABA function causes seizures and that augmentation of GABA function can protect against seizure activity. Direct evidence for altered GABA synaptic markers has been obtained in some animal models of epilepsy, as well as in human focal epilepsy. We present preliminary evidence for a deficit in benzodiazepine receptor binding in the midbrain of seizure-susceptible Mongolian gerbils. These data would be consistent with an impairment of GABA-mediated inhibitory synaptic transmission that contributes to susceptibility to the genesis or spread of seizures in some kinds of epilepsy.

Animals↗