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At least 1,225 records · Page 68Linked to original sources
PubMed1981

Sodium valproate enhancement of gamma-aminobutyric acid (GABA) inhibition: electrophysiological evidence for anticonvulsant activity.

The purpose of this study was to gain further insight into the mechanism of action of the anticonvulsant sodium valproate. The effects of valproate on spontaneous neuronal activity and its interaction with locally applied gamma-aminobutyric acid (GABA) were assessed in the rat cerebral cortex. Extracellular neuronal potentials were recorded using standard procedures. Valproate, glycine, GABA and bicuculline methiodide were applied through microiontophoresis. Valproate at 30, 50, and 100 nA did not affect the spontaneous activity of the majority of cells (21), increased the firing rate in four and slowed right cells. When applied simultaneously with GABA, valproate significantly enhanced GABA inhibition in a dose-related manner. Bicuculline methiodide antagonized the combined effects of valproate and GABA. Glycine inhibitions were not significantly enhanced by valproate. Our results indicate that valproate enhances GABA inhibition in the cerebral cortex, an action which is independent of its effect on spontaneous activity. The specificity of valproate for GABA suggests that this interaction may be an important mechanism through which valproate exerts its anticonvulsant properties.

Action Potentials↗
PubMed1993

Evidence of stimulation of the gamma-aminobutyric acid shunt by valproate and E-delta 2-valproate in neonatal rat brain.

The effect of valproate and its more active metabolite E-delta 2-valproate on the rate of glucose oxidation through different metabolic pathways in neonatal rat brain slices was studied. The presence of valproate or E-delta 2-valproate did not change the rate of [3,4-14C]glucose or [6-14C]glucose incorporation into CO2, suggesting that glucose oxidation through the pyruvate dehydrogenase-catalyzed reaction and through the tricarboxylic acid cycle was not affected by these drugs. However, both drugs significantly enhanced the rate of [2-14C]glucose oxidation, supporting the notion that the activity of the gamma-aminobutyric acid (GABA) shunt is specifically stimulated by valproate and, to a greater extent, by E-delta 2-valproate. The presence of methionine sulfoximine or gamma-hydroxybutyrate did not change the GABA shunt activity. Brain glutamate decarboxylase activity was significantly increased after incubation of the brain slices in the presence of valproate. Consequently, our results suggest that the mechanism of action of valproate is related to the increase in the levels of the inhibitory neurotransmitter GABA caused by the enhancement of flux through the glutamate decarboxylase-catalyzed reaction.

Animals↗
PubMed1989

Uptake of gamma-aminobutyric acid and L-glutamic acid by synaptosomes from postmortem human cerebral cortex: multiple sites, sodium dependence and effect of tissue preparation.

The uptake of gamma-aminobutyric acid (GABA) and L-glutamic acid by synaptosomes prepared from frozen postmortem human brain was shown to be effected via distinct high and low affinity sites. At approximately 17 h postmortem delay, the kinetic parameters for GABA uptake were: high affinity site, Km 7.1 +/- 2.5 microM, Vmax 18.7 +/- 4.8 nmol.min-1 per 100 mg protein; low affinity site, Km 2 +/- 1 mM, Vmax 425 +/- 250 nmol.min-1 per 100 mg protein (means +/- S.E.M., n = 13). Kinetic parameters for L-glutamate uptake were: high affinity site, Km 7.5 +/- 1.0 microM, Vmax 85 +/- 8 nmol.min-1 per 100 mg protein; low affinity site, Km 1.8 +/- 1.2 mM. Vmax 780 +/- 175 nmol.min-1 per 100 mg protein (n = 11). A detailed kinetic analysis of high affinity GABA uptake was performed over a range of sodium ion concentrations. The results were consistent with a coupling ratio of one Na+ ion to one GABA molecule; a similar result was found with rat brain synaptosomes. However, rat and human synaptosomes differed in the degree to which the substrate affinity of the high affinity GABA uptake site varied with decreasing Na+ ion concentration. High affinity GABA uptake was markedly affected by the method used to freeze and divide the tissue, but did not vary greatly in different cortical regions. There was some decline of high affinity GABA uptake activity with postmortem delay, apparently due to a loss of sites rather than a change in site affinity.

Adult↗
PubMed1985

Uptake and release of gamma-aminobutyric acid in the guinea pig cochlear nucleus after axotomy of cochlear and centrifugal fibers.

This study attempts to determine if gamma-aminobutyric acid (GABA) may be a transmitter of cochlear nerve fibers projecting from the cochlea to the cochlear nucleus, and of centrifugal fibers projecting to the cochlear nucleus via the trapezoid body and the acoustic striae of the medulla. The uptake and the electrically evoked release of exogenous [14C]GABA were measured, in vitro, in the three major subdivisions of the guinea pig cochlear nucleus; the anteroventral, posteroventral, and dorsal cochlear nuclei. These activities were compared using unlesioned animals, animals with bilateral cochlear ablations, and animals whose trapezoid body and acoustic striae were interrupted on the right side of the medulla. Subdivisions from unlesioned animals took up [14C]GABA, achieving concentrations in the tissues that were 11-19 times that in the medium. Electrical stimulation evoked a Ca2+-dependent release of [14C]GABA from each subdivision. Bilateral cochlear ablation, which presumably destroyed the cochlear nerve fibers, had no effect on [14C]GABA uptake and release. Section of the trapezoid body and the acoustic striae on the right side of the medulla typically severed all known connections of the right posteroventral and dorsal cochlear nuclei with the rest of the brain, but left intact many connections involved with the right anteroventral cochlear nucleus. This lesion partially depressed [14C]GABA uptake and release in the right posteroventral and dorsal cochlear nuclei, but not in the right anteroventral cochlear nucleus. These findings suggest that one or more of the centrifugal tracts projecting to the cochlear nucleus may be GABAergic, 88% or more of the cochlear nerve fibers probably are not GABAergic, and some neurons of the cochlear nucleus are probably GABAergic.

Animals↗
PubMed2000

Detection of acetylcholinesterase activity and gamma-aminobutyric acid binding sites in Dicrocoelium dendriticum.

In the present study we report the presence of acetylcholinesterase activity and gamma-aminobutyric acid binding sites in crude extracts of Dicrocoelium dendriticum. This indirectly demonstrates the presence of acetylcholine and GABA. The presence of these neurotransmitters could indicate the existence of two systems implicated in the neurotransmission of the Digenea.

Acetylcholinesterase↗
PubMed1983

[Subarachnoid analgesia induced by serotonin and gamma-aminobutyric acid].

It has been shown in experiments on an isolated spinal cord of rats that morphine, serotonin and gamma-aminobutyric acid (GABA) induce the depolarization of the central terminals of primary afferents. The depolarizing effect of morphine is mediated via interneurons, while the similar effect of serotonin and GABA is the result of a direct action on primary afferents. Subarachnoidal injection of morphine (0.1-0.6 mg), serotonin (0.1-0.3 mg) and GABA (0.3-0.6 mg) provokes analgesia upon electric stimulation of the tail root in rats.

Analgesia↗
PubMed1984

Elevation of gamma-aminobutyric acid in human brain may increase dopaminergic neuronal function.

Studies in experimental animals have yielded conflicting findings as to the influence of gamma-aminobutyric acid (GABA) on the activity of nigrostriatal and mesolimbic dopaminergic neurons. We measured cerebrospinal fluid (CSF) concentrations of GABA and homovanillic acid (HVA) in 19 patients before and during treatment with isoniazid. CSF GABA concentrations increased markedly during isoniazid administration, presumably reflecting increases in brain GABA content. At the same time, HVA concentrations in CSF rose significantly. The net effect of elevating brain GABA content in humans appears to be to increase dopamine release from dopaminergic neurons.

Brain↗
PubMed2001

Analysis of extracellular gamma-aminobutyric acid, glutamate and aspartate in cat visual cortex by in vivo microdialysis and capillary electrophoresis-laser induced fluorescence detection.

To investigate the influence of a partial sensory deprivation on the extracellular concentration of amino acid neurotransmitters in cat visual cortex, a capillary electrophoresis method was developed for the quantification of gamma-aminobutyric acid (GABA), glutamate (Glu) and aspartate (Asp) in in vivo microdialysis samples of cat brain. Microdialysis samples from different regions of area 17 were obtained every 15-min using CMA 12 2-mm probes perfused with synthetic cerebrospinal fluid and derivatized using fluorescein isothiocyanate (FITC). Laser-induced fluorescence (LIF) detection was employed. Good selectivity was obtained with a borate buffer (20 mM, pH 10.25). The whole procedure, including the washing step takes only 15 min. The conditions for derivatization and separation were optimized. The parameters for validation such as linearity, precision and detection limit are also reported. The results are consistent with those of HPLC but, as the sample volumes needed are only 1--5 nl, a much better time resolution can be obtained.

Animals↗
PubMed1990

A rapid, sensitive assay for gamma-aminobutyric acid in brain using electron-capture gas chromatography.

A rapid, sensitive procedure has been developed for the assay of gamma-aminobutyric acid (GABA) in brain tissue. The method involves sequential reaction with isobutyl chloroformate and pentafluorophenol under aqueous conditions and subsequent separation and quantitation of the derivative on a gas chromatograph equipped with a capillary column and an electron-capture detector. The method produces a derivative with good stability and provides for simultaneous analysis of GABA and five other aliphaticamino acids in very small volumes of supernatant from brain homogenates.

Amino Acids↗
PubMed1978

Studies on the formation of gamma-aminobutyric acid from putrescine in rat organs and purification of its synthetic enzyme from rat intestine.

The formation of gamma-aminobutyric acid (GABA) from putrescine was examined in organs of rats using radioactive putrescine. Radioactive GABA was detected in all the organs of a rat injected intraperitoneally with radioactive putrescine, and the highest radioactivity of GABA was observed in the small intestine. The enzyme involved in this formation was purified from small intestine and identified as a diamine oxidase, histaminase, from the properties of the enzyme. Activity of the enzyme was found in all the organs of rat, and the highest activity was observed in the small intestine.

Amine Oxidase (Copper-Containing)↗
PubMed1985

Responses to gamma-aminobutyric acid applied to cell bodies and dendrites of rat visual cortical neurons.

The effects of pressure-applied gamma-aminobutyric acid (GABA) on the soma and dendrites of pyramidal and non-pyramidal neurons of rat visual cortical slices were recorded intracellularly. When applied close to the soma, GABA produced hyperpolarizations and depolarizations, but when GABA was applied more than 250 microns from the soma only depolarizations were recorded. The results suggest that most visual cortical cells respond to GABA and that the responses of pyramidal and non-pyramidal cells to GABA are similar.

Animals↗
PubMed1987

Release of endogenous gamma-aminobutyric acid from vocalization nucleus, the robust nucleus of the archistriatum of zebra finch in vitro.

The release of gamma-aminobutyric acid (GABA) from the robust nucleus of the archistriatum (RA) of the zebra finch was examined in slice preparations. Potassium-induced depolarization caused calcium-dependent release of GABA. GABA release by veratrine was blocked by tetrodotoxin. Electrical stimulation of fibers dorsal to RA also released GABA. There was no sex difference in GABA release per wet weight of RA, while the size of the female RA is smaller than that of the male RA.

Animals↗
PubMed1980

Presynaptic actions of 4-aminopyridine and gamma-aminobutyric acid on rat sympathetic ganglia in vitro.

Responses to bath-applications of 4-aminopyridine(4-AP) and gamma-aminobutyric acid (GABA) were recorded intracellularly from neurones in the rat isolated superior cervical ganglion. 4-aminopyridine (0.1-1.0 mmol/l) usually induced spontaneous action potentials and excitatory postsynaptic potentials (EPSPs), which were blocked by hexamethonium. Membrane potential was unchanged; spike duration was slightly increased. Vagus nerve B- and C-fibre potentials were prolonged. In 4-AP solution (0.2-0.3 mmol/l), GABA (0.1 mmol/l), 3-aminopropanesulphonic acid or muscimol evoked "bursts" of spikes and EPSPs in addition to a neuronal depolarization. These "bursts", which were not elicited by glycine, glutamate, taurine or (+/-)-baclofen, were completely antagonised by hexamethonium, tetrodotoxin or bicuculline methochloride. It is concluded that: (a) 4-AP has a potent presynaptic action on sympathetic ganglia; (b) presynaptic actions of GABA can be recorded postsynaptically in the presence of 4-AP; and (c) the presynaptic GABA-receptors revealed in this condition are similar to those on the postsynaptic membrane.

Action Potentials↗
PubMed2005

[The effect of gamma-aminobutyric acid in superoxide dismutase, peroxidase and catalase activity response to salt stress in maize seedling].

Salt stress induced Gamma-aminobutyric acid (GABA) accumulation in maize plants. The germination of maize seeds was inhibited seriously by NaCl treatment, while exogenous GABA reduced the inhibition of NaCl on the seeds germination. Effects on SOD, POD and CAT activity of GABA were detected. 1-2 mmol/L GABA induced the increase of the activity of SOD, POD and CAT about 20%. Because of SOD, CAT and POD are important protective enzymes which can eliminate active oxygen, so GABA can alleviate the damage of salt stress through promoting the activity of the protective enzyme system.

Catalase↗
PubMed1981

Measurement of gamma-aminobutyric acid in human cerebrospinal fluid: radioreceptor assay using [3H]muscimol.

A method is described for the determination of gamma-aminobutyric acid (GABA) levels in human cerebrospinal fluid by modification of the radioreceptor assay utilizing [3H]muscimol as labelled ligand. This method is compared with the radioreceptor assay using [3H]GABA as labelled ligand. Although the [3H]muscimol assay is less sensitive than the [3H]GABA method, it offers the advantage of being more rapid due to the use of a filtration step instead of the usual, more time-consuming centrifugation of the samples. Samples of CSF of patients with various neurological or psychiatric disturbances were analysed. There was a satisfactory correlation between the GABA values obtained by the two assays.

Animals↗
PubMed1986

The "antidementia drug" pantoyl-gamma-aminobutyric acid increases high affinity uptake of choline by slices of rat brain.

Studies were made on the effects of an "antidementia drug", pantoyl-gamma-aminobutyric acid (pantoyl-GABA), on high affinity uptake of choline by slices of rat brain. Depolarization caused by increasing the K+ concentration to 25 mM for 30 min before incubation with [3H]choline enhanced the uptake of radioactivity by slices of cerebral cortex, hippocampus and striatum during a 5 min incubation in the presence of 1 microM [3H]choline. Pantoyl-GABA (1 mM) increased the depolarization-induced uptake of radioactivity by the slices of cortex and hippocampus, but not by the slices of striatum; it had little effect on the uptake when the slices were not depolarized. It also had no effect when the slices were depolarized in the incubation medium without Ca2+. Since the high affinity uptake of choline is considered to be a regulatory step in the synthesis of acetylcholine (ACh), these results suggest that pantoyl-GABA increases the synthesis of ACh in cholinergic terminals in the cerebral cortex and hippocampus. This action may be involved in its effect as an antidementia drug, because cholinergic deficits are assumed to occur in Alzheimer's disease.

Alzheimer Disease↗
PubMed1983

Simultaneous determination of leu-enkephalin localization and [3H] gamma-aminobutyric acid uptake in rat striatal cell cultures.

The purpose of this study was to investigate the coexistence of gamma-aminobutyric acid (GABA) and leu-enkephalin in single neurons from the corpus striatum. Monolayer cell cultures, started from newborn rat corpus striatum, were grown in serum-free medium and examined using GABA autoradiography and leu-enkephalin immunocytochemistry in a double-label protocol. Examples of cells were found which were positive for one or the other neurotransmitter or for neither transmitter, but not for both. Furthermore, cells which appear similar by morphological criteria alone differed in transmitter specificity. We conclude that the two transmitters tested are not localized within single cells and that morphology alone is inadequate to identify functional cell classes in this area.

Animals↗
PubMed1980

Autoradiographic localization of gamma-aminobutyric acid (GABA) receptors in the rat cerebellum.

[3H]Muscimol was used in the light microscopic autoradiographic localization of gamma-aminobutyric acid (GABA) receptors in the rat cerebellum. The binding of [3H]-muscimol to the slide-mounted tissue sections had all of the characteristics associated with a GABA receptor. It was saturable with appropriate kinetic constants and was blocked only by other GABAergic drugs. Autoradiographic studies revealed a very high density of receptors over the granule cell layer, a low level over the molecular layer, and negligible receptor binding over white matter. This suggested a high localization of GABA receptors to granule cells, which is supported by other neurochemical studies. The autoradiographic procedure used here should be a useful method in further studies of receptors requiring high sensitivity and increased anatomical resolution.

Animals↗