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[Blood level of gamma-aminobutyric acid--"peripheral index" of the state of central neuromediator system].

The review summarized data on contents of the main inhibitory neurotransmitter of the central nervous system: gamma-aminobutyric acid (GABA) in blood of normal animal and humans, in blood of different animal species under experimental effects and modelling of pathological states, as well as in human blood in the presence nervous and endocrine diseases. Determination of GABA concentration in blood, taking into account the accessibility of study object, absence of significant sex, age, seasonal, diurnal fluctuations, as well as stability of amino acid level during the laboratory assay procedure, may be useful for the study of central neuromediator mechanisms, and allows, using representative samples and corresponding groups of comparison, to obtain data on disturbances of functional state of the GABAergic system under conditions of brain pathology.

Animals↗
PubMed1995

Anti-stress activity of N-phthaloyl gamma-aminobutyric acid in rats.

The effect of immobilization restraint stress (RS) on some biochemical and biophysical parameters in rats and their modulation by N-phthaloyl gamma-aminobutyric acid (P.GABA) was studied. RS did not affect the levels of serum Ca2+, inorganic phosphate, bilirubin, total protein, but caused insignificant increase of albumin level and significantly decreased the cholesterol level. This RS induced decrease of serum cholesterol level was reversed by prior treatment with P.GABA, while the albumin content showed a decrease. RS-induced a generalised increase in serum enzyme activity of lactate dehydrogenase (LDH), alkaline phsophatase (AIP), serum glutamate pyruvate transaminase (SGPT) and serum glutamate-oxaloacetate transaminase (SGOT). P.GABA normalised RS-induced increase of LDH and AlP activity, but it further enhanced SGOT and SGPT activities. In synaptosomal membranes, RS caused a decrease in clusterization and fluidity, but the thickness of the membrane increased as studied by fluorescence probes. Prior administration of P.GABA normalised the changes observed in the synaptic membrane.

Animals↗
PubMed1984

gamma-aminobutyric acid B receptors are negatively coupled to adenylate cyclase in brain, and in the cerebellum these receptors may be associated with granule cells.

Baclofen and gamma-aminobutyric acid (GABA) are shown to inhibit basal adenylate cyclase activity in brain of rat. The response is mediated through the GABAB receptor, and the rank order of potency for agonists is (-)-baclofen (EC50 = 4 microM) greater than GABA (EC50 = 17 microM) greater than muscimol greater than (+)-baclofen. GABAA agonists are not effective inhibitors of cyclase activity. The response is bicuculline-insensitive, and diazepam does not modify the GABA or (-)-baclofen inhibition of adenylate cyclase. Studies with neurologically mutant mice correlated a loss in GABAB receptor-mediated inhibition of cyclase with a loss in cerebellar granule cells. Thus, the GABAB receptor is negatively coupled to adenylate cyclase in various brain areas, and, in the cerebellum, data suggest a granule cell localization of this activity.

Adenylyl Cyclases↗
PubMed1988

Importance of glutamine for gamma-aminobutyric acid synthesis in rat neostriatum in vivo.

This work was carried out to evaluate the importance of glial cells in providing precursors for the in vivo synthesis of gamma-aminobutyric acid (GABA). Fluorocitrate, which selectively inhibits the tricarboxylic acid cycle in glial cells, was administered locally in rat neostriatum. Inhibition of the glial cell tricarboxylic acid cycle led to a decrease both in glutamine level and in gamma-vinyl GABA (GVG)-induced GABA accumulation, an observation indicating reduced GABA synthesis. The role of glutamine, which is synthesized in glial cells as a precursor for GABA, was further investigated by inhibition of glutamine synthetase with intrastriatally administered methionine sulfoximine. In this case, the glutamine level was reduced to near zero values, and the GVG-induced GABA accumulation was only half that of normal. The results show that glutamine is an important precursor for GABA synthesis, but it cannot be the sole precursor because it was not possible to depress the GVG-induced GABA accumulation completely.

Aminocaproates↗
PubMed1988

Enhancement of t-[35S]butylbicyclophosphorothionate and [3H]strychnine binding by monovalent anions reveals similarities between gamma-aminobutyric acid- and glycine-gated chloride channels.

The characteristics of [3H]strychnine and t-[35S]-butylbicyclophosphorothionate ([35S]TBPS) binding to sites associated with glycine- and gamma-aminobutyric acid (GABA)-gated chloride channels were compared in the presence of a series of anions with known permeabilities through these channels. Good correlations were found between (a) the potencies (EC50) of these anions to stimulate radioligand binding and their permeabilities relative to chloride; (b) the affinities (KD) of these radioligands in the presence of fixed concentrations of these anions and their relative permeabilities; (c) the potencies (EC50) of these anions to stimulate [35S]TBPS and [3H]strychnine binding; and (d) the affinities (KD) of [3H]strychnine and [35S]TBPS measured at a fixed concentration of these anions. These studies support electrophysiological and biochemical observations demonstrating similarities between glycine- and GABA-gated chloride channels, and suggest that anions enhance [3H]strychnine and [35S]TBPS binding through specific anion binding sites located at the channels.

Animals↗
PubMed1997

The interactions of hexachlorocyclohexane isomers with human gamma-aminobutyric acid(A) receptors expressed in Xenopus oocytes.

The effects of gamma-hexachlorocyclohexane (gamma-HCH) and its alpha, beta and delta isomers on the gamma-aminobutyric acid (GABA) responses of human alpha1beta3gamma2S and alpha6beta3gamma2S GABA(A) receptors expressed in Xenopus oocytes were examined by conventional two-electrode voltage-clamp techniques. Gamma-HCH induced partial inhibition of EC50 GABA responses, whereas the alpha and delta isomers produced potentiation of EC20 GABA currents. In contrast, beta-HCH had no effect on GABA currents, even at concentrations as high as 100 microM. The effects of the active HCH isomers were not influenced by alpha subunit composition because there was no significant difference in either the inhibition or potentiation of alpha1beta3gamma2S or alpha6beta3gamma2S GABA(A) receptors. Delta- and gamma-HCH antagonized picrotoxin inhibition and caused displacement of specific [35S]t-butylbicyclophosphorothionate binding. Delta-HCH potentiation was found to be additive with steroid, loreclezole and lanthanum potentiation, but nonadditive with potentiation by pentobarbital and propofol, which suggested that its activity was linked to the barbiturate site.

Animals↗
PubMed1993

Quantitative analyses of the coexistence of gamma-aminobutyric acid in substance P-amacrine cells of the larval tiger salamander retina.

The present study was performed as part of a systematic examination of gamma-aminobutyric acid's (GABA) coexistence with other classical transmitters and neuropeptides in neuronal populations of the larval tiger salamander retina. Substance P immunocytochemistry was combined with either GABA immunocytochemistry or autoradiography of high-affinity GABA uptake to examine for the presence of GABA in substance P-amacrine cells of the larval tiger salamander retina. Double-label analyses revealed two populations of substance P-amacrine cells that express both markers of GABA activity. One population was situated in the innermost cell row of the inner nuclear layer, while the other population was located in the ganglion cell layer. In both cases, these double-labelled cells accounted for approximately 10% of substance P-amacrine cells in their respective layers. The present study demonstrates, therefore, that substance P-amacrine cells in the larval tiger salamander retina can be categorized on the basis of their coexisting/non-coexisting relationships with GABA and suggests a possible functional diversity in the population of substance P-amacrine cells.

Ambystoma↗
PubMed1983

Further investigations on brain distribution of hydrazine and its gamma-aminobutyric acid elevating effect in rats.

Perry's hypothesis that hydrazine (Hz) derived from isoniazid (INH) treatment plays an important role in the elevation of brain gamma-aminobutyric acid (GABA) levels was reexamined by measuring Hz and GABA levels in the brain after the treatment with 50 mg/kg of INH or different doses of Hz. The treatment with 50 mg/kg of INH to rats resulted in the elevation of GABA levels in rat whole brain. The maximum levels of GABA increased about twice at 4 h from 2.06 +/- 0.4 mumol/g wet wt. in the control group to 3.61 +/- 0.4 mumol/g wet wt. in INH treated group. In this case, brain levels of Hz ranged from 25.6 to 80.8 ng/g wet wt. within 10 h. On the other hand, Hz levels after the treatment with 0.5 mg/kg of Hz were about five times higher than those after INH treatment. However, 0.5 mg/kg of Hz treatment did not increase brain GABA levels at all. Perry's hypothesis was denied by the fact that brain Hz levels after INH treatment were too low to elevate brain GABA levels.

Animals↗
PubMed2000

The inhibitory effects of (gamma)-aminobutyric acid (GABA) on growth hormone secretion in the goldfish are modulated by sex steroids.

Double-labelling studies at the electron microscopic level demonstrated that gamma-aminobutyric acid (GABA)-immunoreactive nerve endings are associated with growth-hormone-secreting cells in the proximal pars distalis of the goldfish pituitary gland, suggesting that GABA may be important for the control of growth hormone release in this species. An in vitro assay for GABA-transaminase activity demonstrated that the pituitary is a site for the metabolism of GABA to succinic acid. In vitro, GABA or the GABA antagonists bicuculline and saclofen did not affect the rate of growth hormone release from dispersed pituitary cells in static incubation. In contrast, intracerebroventricular injection of GABA reduced serum growth hormone levels within 30 min. During the seasonal gonadal cycle, intraperitoneal injection of GABA was without effect in sexually regressed goldfish, but caused a significant decrease in serum growth hormone levels in sexually recrudescent animals. Intraperitoneal implantation of solid silastic pellets containing oestradiol increased serum GH levels fivefold in sexually regressed and recrudescent goldfish; in both groups, GABA suppressed the oestradiol-stimulated increase in circulating growth hormone levels. The effect of oestradiol on basal serum growth hormone levels was specific since progesterone and testosterone were without effect. However, in recrudescent animals treated with progesterone and testosterone, the inhibitory effects of GABA on serum growth hormone levels were absent, indicating a differential role for these steroids in growth hormone release. Taken together, these results demonstrate that GABA has an inhibitory effect on growth hormone release in goldfish.

4-Aminobutyrate Transaminase↗
PubMed1989

[Effects of the stimulation of D1 and D2 dopaminergic receptors on the electrically induced release of gamma-(3H)-aminobutyric acid in the prefrontal cortex of the rat].

The effects of D1 and D2 dopaminergic agonists and antagonists on the electrically-evoked release of gamma-[3H] aminobutyric acid (3H-GABA) have been studied on rat prefrontal cortex slices. The major part of the electrically-evoked release of 3H-GABA appeared to be Ca++ dependent since a 62% decrease was observed when calcium was removed from the superfusion medium. Two specific D2 dopaminergic agonists, RU 24926 (10(-7) M) and lisuride (10(-6) M), respectively induced a 32% and a 50% inhibition of the electrically-evoked release of 3H-GABA. The selective D2 dopaminergic antagonists sulpiride (10(-5) M) totally abolished the effect of RU 24926 and partially abolished the effect of lisuride. The selective D1 agonist SKF 38393 (10(-5) M) did not affect 3H-GABA release. These results suggest that in the rat prefrontal cortex in vitro, the dopaminergic modulation of 3H-GABA release is mediated through D2 but not D1 receptors. The activation of D2 dopaminergic receptors induces an inhibition of the electrically-evoked release of 3H-GABA.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Ethanol potentiates the effect of gamma-aminobutyric acid on medial vestibular nucleus neurons responding to horizontal rotation.

Electrophysiological studies were performed to determine whether or not ethanol potentiates the inhibitory effects of gamma-aminobutyric acid (GABA) on medial vestibular nucleus (MVN) neurons responding to horizontal sinusoidal rotation using alpha-chloralose anesthetized cats. The MVN neurons were classified into types I, II, III and IV neurons according to the responses to the horizontal rotation of the animal placed on the turntable in directions ipsilateral and contralateral to the recording site. In addition, the effects of ethanol and GABA on type I neurons were also examined. Micro-osmotic application of ethanol up to 100 nA did not affect the spontaneous firing or the rotation-induced increase in firing of type I neurons. However, the inhibitory effects of GABA up to 50 nA on the rotation-induced increase in firing were potentiated during simultaneous application of ethanol up to 100 nA. This potentiated inhibition was blocked by iontophoretic application of bicuculline (25-150 nA) and picrotoxin (45-150 nA). These results suggest that ethanol potentiates the inhibitory effects of GABA on MVN type I neurons by acting on the GABA receptor and/or receptor-coupled chloride ion channel.

Animals↗
PubMed1995

Determination of gamma-aminobutyric acid levels in human cerebrospinal fluid using Pseudomonas.

The principle objective was to demonstrate the efficacy of a bacterial, radioligand, competitive binding method in determining gamma-aminobutyric acid (GABA) levels in human cerebrospinal fluid (CSF). In a double blind study, CSF GABA concentrations were measured by the bacterial method using a mutant of Pseudomonas fluorescens and by a standard radioligand competitive binding assay using rat brain membranes. Linear regression analysis demonstrated a highly significant correlation (r = 0.84; P < 0.001) between the two methods. In an ancillary study, a similar correlation (r = 0.90; P < 0.001) was found between the bacterial method and HPLC, another standard procedure in determining CSF GABA levels. Furthermore, the mean CSF GABA measurements found with the bacterial method were in agreement with those reported in the literature using the brain membrane method or HPLC. The bacterial method was highly reproducible and reliable with a detection to 5 nM GABA. It was specific for GABA and was not affected by other naturally occurring compounds which are found in higher concentrations in CSF than GABA or which were suspected to interfere with the neurotransmitter in a binding assay. The bacterial radioligand method was shown to be an accurate, sensitive, and rapid assay for CSF GABA.

Adult↗
PubMed1997

Dependence of gamma-aminobutyric acid modulation of cholinergic transmission on nitric oxide and purines in cat terminal ileum.

The possible involvement of purines and/or nitric oxide (NO) in the gamma-aminobutyric acid (GABA)A receptor-mediated effects on the spontaneous activity of isolated preparations from longitudinal and circular muscles of cat terminal ileum was investigated. GABA had biphasic effects, which were neurogenic and muscarinic. ATP and adenosine dose dependently inhibited the activity of the muscles. A contractile response evoked by the nucleotide only was also observed. The effects of the purines were equipotent and resistant to Nomega-nitro-L-arginine (L-NNA), tetrodotoxin and to desensitization by alpha,beta-methylene adenosine 5'-triphosphate (alpha,beta-meATP), except for the contractile effect of ATP, which was abolished by alpha,beta-meATP. Pretreatment of the preparations with ATP or adenosine produced: (i) desensitization to the effects of the respective purinoceptor agonist only; and (ii) suppression of the GABA-induced responses of longitudinal and circular muscles. Hemoglobin and L-NNA greatly reduced or completely blocked the GABA(A)-induced relaxation and decreased the GABA(A)-induced contraction. Our results indicate that purines and NO, to a different extent, mediate the relaxant phase of the GABA effects in both layers. Interactions between muscarinic cholinoceptors and GABA-nitrergic pathway and a concomitant activation of postjunctional P1 and P2y purinoceptors are suggested to explain the prejunctional biphasic effects of GABA.

Adenosine↗
PubMed1988

Quantitative comparisons of gamma-aminobutyric acid neurons and receptors in the visual cortex of normal and dark-reared cats.

Physiological studies suggest that the function of the visual cortical gamma-aminobutyric acid (GABA) system is abnormal in cats reared in total darkness. The present study asked whether visual input is necessary for the normal postnatal anatomical development of the GABA system by comparing GABA neurons and receptors in the visual cortex of normal and dark-reared cats. Immunohistochemical techniques (anti-GABA) were used to localize GABA neurons. In both rearing conditions, GABA neurons were stained rather uniformly in all cortical layers. Counts of GABA cells indicated a marked increase in density in dark-reared compared to normal cats. Counts of total cellular density in cresyl-stained sections, however, indicated a comparable increase in dark-reared cats. When corrected for total cellular density, there were no differences between dark-reared and normal cats in the density of GABA cells per layer, or the relative proportion of GABA cells across cortical layers. In vitro receptor binding of 3H-muscimol was used to compare GABAA receptors in the two rearing conditions. When corrected for total cellular density, saturation kinetics indicated no difference in the total number or affinity of receptors. Similarly, autoradiographic histology indicated no difference in the laminar distribution of receptors across cortical layers between dark-reared and normal cats. These results indicate that the postnatal development of GABA neurons and receptors occurs normally in the absence of visual input.

Aging↗
PubMed1979

Bidirectional movement of gamma-aminobutyric acid in cerebral cortex slices incubated in small volumes of medium.

Rat cerebral cortex slices were incubated in small volumes of medium in order to study the bidirectional movements of gamma-aminobutyric acid (GABA) between tissue and medium, and to measure the extent of release of endogenous amino acids of interest as potential neurotransmitters. The apparent uptake, real uptake, and net change of GABA were calculated from the changes in [14C]GABA and endogenous GABA in the medium. The extent of release of endogenous amino acids was dependent upon the amino acid the duration of incubation, and the volume of incubating medium. Substantial amounts of endogenous amino acids may accumulate in the medium under conditions commonly employed in amino acid uptake studies. The accumulation of endogenous GABA may affect the calculation of GABA uptake when this is based on the initial specific activity of exogenous [14C]GABA. The difference between apparent uptake and real uptake was particularly prominent in the presence of the depolarizing agents, potassium or veratridine, which caused a marked increase in GABA release. Exchange or net release of GABA was found when slices were incubated briefly in media containing 1.3 micrometer or 12.5 micrometer exogenous GABA; net uptake accounted for 50% of observed uptake when slices were incubated in media containing 25 micrometer GABA.

Amino Acids↗
PubMed1985

Lipid peroxidation-induced inhibition of gamma-aminobutyric acid uptake in rat brain synaptosomes: protection by glucocorticoids.

Incubation of rat brain synaptosomes with xanthine and xanthine oxidase (X/XO) resulted in an inhibition of gamma-aminobutyric acid (GABA) uptake. The inhibitory effects of X/XO were temperature- and time-dependent, and were characterized by an increased Km for GABA and a decreased Vmax. Inhibition of GABA uptake by X/XO was associated with both the formation of malonyldialdehyde (MDA) and conjugated dienes, indicating that lipid peroxidation was involved. Studies with catalase, superoxide dismutase (SOD), mannitol, and chelated iron suggested that hydroxyl radical (OH X) was probably responsible for the initiation of lipid peroxidation. Both the peroxidation of synaptosomal membranes and the inhibition of GABA uptake by X/XO were enhanced by the addition of ADP and FeCl2. The X/XO-induced inhibition of GABA uptake by synaptosomes could be prevented by preincubation of synaptosomes with certain glucocorticoids prior to X/XO exposure. Methylprednisolone sodium succinate (MPSS), dexamethasone sodium phosphate (DMSP), and prednisolone sodium succinate (PSS) all prevented the inhibition of GABA uptake by X/XO. MPSS was most effective at concentrations around 100 microM, DMSP was slightly more potent, and PSS was optimal at around 300 microM. On the other hand, hydrocortisone sodium succinate (HCSS) was ineffective at preventing X/XO-induced inhibition of GABA uptake at concentrations up to 3 mM. The steroids are presumed to work through a mechanism that blocked the formation of lipid peroxides, as MPSS inhibited the formation of conjugated dienes in synaptosomes exposed to X/XO at a concentration that also protected GABA uptake.

Animals↗
PubMed2001

[The effect of gamma-aminobutyric acid injected into lateral brain ventricle of rats after prenatal cadmium intoxication on flash visual evoked potentials (FVEP)].

PURPOSE: To find out any influence of gamma-aminobutyric acid (GABA) injected into lateral brain ventricle in newborn rats prenatally exposed to cadmium (Cd). METHOD: 18 white, Wistar, offspring rats were divided into 3 groups, each consisting of 6 rats (control, 5 ppm and 50 ppm of Cd in drinking water). Newborns were examined when they were 3-6 months old. FVEP were recorded before and after GABA injections. Two doses of GABA were used, 10 and 100 nmols. The statistic analysis with the test of t-Student was performed to estimate the amplitudes and latencies of the negative wave N1 and the next positive one P2. p < 0.05 was used to indicate significant difference. RESULTS: No significant changes in the latencies of peak N1 and P2 in the control and Cd 5 ppm groups (101-103%) after 10 nmols GABA were observed. However, the shortened (91-97%) of them was observed after both doses of GABA in Cd 50 ppm group. The mean value of amplitude of N1 in control rats increased to 127% after 10 nmols GABA and 142% after 100 nmols GABA. Moreover, the mean amplitude of P2 in this group increased to 108% and 146%, respectively. The high significant increase of the amplitudes of N1 (181-280%) and P2 (160-177%) waves were received after both doses of GABA in Cd groups. CONCLUSION: Cadmium increased the sensitivity of GABA-receptors in the OUN.

Animals↗
PubMed1989

In vivo conversion of gamma-aminobutyric acid and 1,4-butanediol to gamma-hydroxybutyric acid in rat brain. Studies using stable isotopes.

The formation of 4-[1,4-13C]hydroxybutyric acid ([13C]gamma-hydroxybutyric acid; [13C]GHB) in rat brain was studied following intracerebroventricular (i.c.v.) administration of either 4-[1,4-13C]aminobutyric acid ([13C]GABA or 1,4-[1,4-13C]butanediol ([13C]1,4-BD) to awake, freely moving animals. GHB and [13C]GHB were measured with a gas chromatographic mass spectrometric (GC/MS) technique designed to detect the lactone derivative of GHB with the acid or lactone being determined by conditions of tissue extraction. [13C]GHB was detected following i.c.v. administration of [13C]GABA with a turnover rate of 2.04 nmol/g tissue/hr and [13C]1,4-BD with a turnover rate of 1.4 nmol/g/hr. The formation of [13C]GHB from [13C]GABA was blocked by an inhibitor of GABA-transaminase, but this drug had no effect on the formation of [13C]GHB from [13C]1,4-BD. The latter pathway was also unaffected by alcohol dehydrogenase inhibitors, compounds which block this pathway in the periphery. Further, in the course of these experiments, naturally occurring endogenous gamma-butyrolactone (GBL) was detected in rat brain in a concentration of 200 pmol/g tissue weight, but lactonization in vivo of [13C]GHB formed from either labeled GABA or 1,4-BD was not demonstrated. These data confirm two separate pathways of synthesis for GHB in brain, demonstrate the presence of GBL in brain, and illustrate the utility of a new GC/MS technique for analysis of GHB and for GBL which does not involve extensive derivatization.

Animals↗