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PubMed1988

Uptake of gamma-aminobutyric acid by a synaptic vesicle fraction isolated from rat brain.

Gamma-Aminobutyric acid (GABA) was taken up by a MgATP-dependent mechanism into synaptic vesicles isolated by hypoosmotic shock and density gradient centrifugation. The properties of the vesicular uptake differed clearly from those of synaptosomal and glial uptake, both with respect to Na+, Mg2+, and ATP dependence and with respect to response to general GABA uptake inhibitors such as nipecotic acid, diaminobutyric acid, and beta-alanine. The uptake showed a Km of 5.6 mM and a net uptake rate of 1,500 pmol/min/mg of protein. It is suggested that the vesicular uptake of GABA is driven by an electrochemical proton gradient generated by a Mg2+-ATPase.

Adenosine Triphosphate↗

PubMed1991

A method for culturing rat oviduct gamma-aminobutyric acid cells.

A technique for the culture of rat oviduct gamma-aminobutyric acid (GABA) cells is described. The technique involves first explaining the fimbria and preampulla, which are the oviduct divisions with the highest density of GABA cells. The explanted tissue is cultured in a serum-free medium, to propagate the outgrowing cells. Under the experimental conditions we describe, the majority of the cells maintain GABA expression, as determined by immunostaining with a GABA antiserum.

Animals↗

PubMed1977

Development of spontaneous motility in chick embryos. Inhibitory effect of glycine and gamma-aminobutyric acid.

The effect of glycine (100 mg/kg egg weight) and gamma-aminobutyric acid (GABA, 103 mg/kg egg weight) on spontaneous motility was studied in chick embryos from the 11th to 21st day of incubation. Neither substance affected 11- and 13-day embryos (except for transient augmentation of spontaneous motility in some of the 13-day embryos after glycine). From the 15th day of incubation, both substances inhibited spontaneous motility, the effect being most pronounced in 17-day embryos. Their effect on 21-day embryos was weaker than their effect on younger embryos. The results are evaluated as evidence of later maturation of inhibitory mechanisms during development of the chick embryo CNS.

Aminobutyrates↗

PubMed1977

The central action of gamma-aminobutyric acid in rats.

The influence of 100--600 microng of gamma-aminobutyric acid (GABA) injected into the right lateral ventricle of the brain on behavior and activity of the cerebral cholinergic system was studied in Wistar rats. Proportionally to dosage, GABA inhibited motor and exploratory activity in the rats. Reduction in the content of acetylcholine in the pons and medulla oblongata was accompanied by increased acetylcholinesterase (AChE) activity. GABA changed AChE activity differently in various parts of the brain. GABA depressed motor and exploratory activity in rats in a degree dependent on its dosage and inborn exploratory of the rats, and this effect was accompanied by changes in the cerebral cholinergic system.

Acetylcholine↗

PubMed1985

gamma-Aminobutyric acid concentrations are maintained in anoxic turtle brain.

Changes in gamma-aminobutyric acid (GABA) concentrations in the turtle (Pseudemys scripta elegans) brain were studied in situ during prolonged anoxia. With the onset of anoxia, the well-documented rapid increases in GABA found in mammalian brains were not observed in the turtle brain. Although not statistically significant, mean GABA concentrations in the turtle brain were reduced from anesthetized control values during the first 30 min of anoxia. During this initial period brain glutamate content declined. Even after 2 h of nitrogen respiration, GABA in the turtle brain still did not rise above control levels. By the 4th h of anoxia, however, GABA had increased to 147% of control values.

Adenosine Triphosphate↗

PubMed1985

Brain gamma-aminobutyric acid and benzodiazepine receptor binding in dialysis encephalopathy.

We measured gamma-aminobutyric acid (GABA) and benzodiazepine binding in autopsied frontal cortex of 8 patients dying with dialysis encephalopathy (DE). No alteration in [3H] GABA binding was observed. However, a mild reduction (-23%, P less than 0.05) of [3H] flunitrazepam-binding density was found in DE cortex. The magnitude of this reduction was similar to that observed in frontal cortex of amygdala-kindled rats [10]. We suggest that a reduction in benzodiazepine receptor number, in combination with markedly reduced GABA concentration in DE cerebral cortex may contribute to some of the clinical features (especially seizures) characteristically observed in this syndrome.

Benzodiazepinones↗

PubMed1999

A single hydrophobic residue confers barbiturate sensitivity to gamma-aminobutyric acid type C receptor.

Barbiturate sensitivity was imparted to the human rho1 homooligomeric gamma-aminobutyric acid (GABA) receptor channel by mutation of a tryptophan residue at position 328 (Trp328), which is located within the third transmembrane domain. Substitutions of Trp328 with a spectrum of amino acids revealed that nearly all hydrophobic residues produced receptor channels that were both directly activated and modulated by pentobarbital with similar sensitivities. Previous studies with ligand-gated ion channels (including GABA) have demonstrated that even conservative amino acid substitution within the agonist-dependent activation domain (N-terminal extracellular domain) can markedly impair agonist sensitivity. Thus, the lack of significant variation in pentobarbital sensitivity among the Trp328 mutants attests to an intrinsic difference between pentobarbital- and the GABA-dependent activation domain. Compared with the heterooligomeric alphabetagamma receptor channel, the mode of modulation for homooligomeric Trp328 mutants by pentobarbital was more dependent on the GABA concentration, yielding potentiation only at low concentrations of GABA (fractions of their respective EC50 values), yet causing inhibition at higher concentrations. Agonist-related studies have also demonstrated that residue 328 plays an important role in agonist-dependent activation, suggesting a functional interconnection between the GABA and pentobarbital activation domains.

Amino Acid Sequence↗

PubMed1995

Modulatory actions of gamma aminobutyric acid (GABA) on GABA type A receptor subunit expression and function.

Gamma aminobutyric acid (GABA) is present in the central nervous system (CNS) during very early embryogenesis. It is therefore likely to play a role not only as a neurotransmitter but also as a signal molecule for neuronal differentiation, growth, and development. It has been firmly established that formation of synapses is strengthened by GABA, and the expression of certain subunits of the GABA type A (GABAA) receptor complex is clearly promoted by GABA. This latter effect of GABA may have profound implications for the functional activity of GABAergic synapses since the pharmacological properties of GABAA receptors are governed by the subunit composition of the receptor complex. Dynamic changes in GABAA receptor expression and diversity during development and differentiation may therefore play important roles for the inhibitory potential of the CNS during mature stages.

Animals↗

PubMed1996

Activation of the cannabinoid receptor by delta 9-tetrahydrocannabinol reduces gamma-aminobutyric acid uptake in the globus pallidus.

The interaction between GABA (gamma-aminobutyric acid) and cannabinoids in the globus pallidus was investigated by evaluating the effects of delta 9-tetrahydrocannabinol on [3H]GABA uptake into slices of rat globus pallidus. delta 9-Tetrahydrocannabinol caused a concentration-dependent decrease in GABA uptake (51% decrease at 100 microM delta 9-tetrahydrocannabinol, IC50 = 18.95 microM). This effect was reversed in a concentration-dependent manner (IC50 = 11.9 microM) by the cannabinoid receptor antagonist SR 141716A (N-(piperidin-1-yl-)5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1 H-pyrazole-3-arboxiamidehydrochloride. SR 141716A alone did not affect GABA uptake. These results show that cannabinoid receptor activation reduces GABA uptake in the globus pallidus.

Animals↗

PubMed1992

Low plasma gamma-aminobutyric acid levels in male patients with depression.

Plasma levels of gamma-aminobutyric acid (GABA) were significantly lower in males with primary unipolar major depressive disorder than in healthy controls. Although the difference in means between control and symptomatic depressed patient groups was small, the distribution of plasma GABA in the depressed patients was markedly different from controls. Forty percent of depressed patients had plasma GABA levels below those of controls. Plasma GABA levels correlated positively with duration of illness, and negatively with age at onset of the mood disorder and the total Endogenomorphic Symptom Score on the Hamilton Rating Scale. Plasma GABA levels may be a biochemical marker of vulnerability to depression, as opposed to a consequence of the illness. A low GABA condition in depression fits and complements the prevailing biogenic amine hypotheses of depression.

Adult↗

PubMed1989

gamma-Aminobutyric acid uptake by a bacterial system with neurotransmitter binding characteristics.

gamma-Aminobutyric acid (GABA), an amino acid, has been found in every class of living organisms. In higher organisms, GABA is a neurotransmitter and binds with high affinity and specificity to GABA receptors on neurons in a sodium-independent reaction that is saturable. The role of GABA in organisms lacking nervous tissue is not known. This report describes, in a strain of Pseudomonas fluorescens, a GABA uptake system with binding characteristics like those of the GABA (type A) brain receptor. The binding was saturable and specific for GABA, was sodium-independent, was of high affinity (Km = 65 nM), and was inhibited competitively by muscimol, a potent GABA analogue. The bacterial GABA system included a homogeneous binding site, and no cooperative interaction was found between sites. To our knowledge, such a system for GABA, or other neurotransmitters, in a bacterium has not been reported.

Binding, Competitive↗

PubMed1996

gamma-Aminobutyric acid: a novel tetragonal phase.

In the tetragonal phase of gamma-aminobutyric acid, C4H9NO2, the single type of molecule adopts a partially folded zwitterionic form. Whereas in the previously characterized monoclinic phase the partially folded zwitterionic molecules exhibit a gauche conformation with respect to the C2-C3 bond, in this phase the molecules exhibit a trans conformation. The altered pattern of intramolecular N...O distances may be of significance with respect to the neurotransmission behavior of this substance. In addition to three strong hydrogen bonds involving the three H atoms bound to the N atom, as in the monoclinic phase, there is a fourth weaker one which results in a two-center bifurcated bond. There is also evidence suggestive of an intramolecular bridging hydrogen bond involving the N atom, an O atom and a methylene H atom, as previously proposed as a stabilizing factor for the gauche conformation observed in the monoclinic phase.

Crystallography, X-Ray↗

PubMed1980

Levels of gamma-aminobutyric acid in cerebrospinal fluid in various neurologic disorders.

Levels of gamma-aminobutyric acid (GABA) in CSF were measured by the ion exchange-fluorometric method in 136 patients who underwent evaluation for neurologic disorders. In 19 patients with no organic neurologic or mental disorders who acted as normal controls, the mean (+/-SD) GABA level in CSF was 239 +/- 76 picomoles/mL. Patients with acute hypoxic encephalopathy showed a mean GABA level in CSF higher than that of the controls, a difference that was statistically significant. In all the other disorders studied, the mean GABA level in CSF was either equal to or lower than that found in the controls. Statistically significant reductions of the GABA level in CSF were seen in patients with Huntington's disease, dementias, cerebellar cortical atrophy, multiple sclerosis, epilepsy, and Parkinson's disease.

Brain Chemistry↗

PubMed1984

The nature of the stimulatory action of gamma-aminobutyric acid in the isolated perfused dog adrenals.

The effect of gamma-aminobutyric acid (GABA) on catecholamine (CA) release from adrenal medulla was investigated. GABA and GABA agonists, 3-amino-1-propane-sulfonic acid and imidazole-4-acetic acid caused CA release from isolated perfused dog adrenals in a dose-dependent manner, and no tachyphylaxis to GABA was observed. CA release elicited by GABA was antagonized by bicuculline and picrotoxin. This antagonism was specific for GABA- and GABA agonist-induced responses, response to acetylcholine being unaffected. Pretreatment with atropine plus hexamethonium did not affect the response to GABA. GABA-induced CA release was abolished by the removal of Ca2+ from perfusion medium, but not by the removal of Na+ or Cl-. Verapamil, CoCl2 and dibucaine blocked the effect of GABA. A Na+ channel blocker, tetrodotoxin did not reduce GABA-evoked CA release. These results suggest that GABA may interact with its receptor to evoke CA release from adrenal medulla in a fashion of Ca2+-dependence and independence on external Na+ or Cl-.

Acetylcholine↗

PubMed1990

Butyrylcholinesterase fluctuation in male albino rats with intracerebroventricular injection of gamma aminobutyric acid, muscimol, and picrotoxin.

The effects of intracerebroventricular injection of gamma-Aminobutyric acid, muscimol, or picrotoxin have been studied on butyrylcholinesterase (BuChE) activities in the serum and several hypothalamic nuclei using biochemical, histochemical, and cytophotometric techniques, respectively. The blood samples were withdrawn from indwelling catheters in jugular vein 1, 15, 30, 45, 60, 90, and 120 min after injection of the drugs. Biochemical estimations demonstrated a significant inhibition of BuChE after GABA and muscimol injections, whereas a pronounced stimulation of BuChE was observed after injection of picrotoxin. The peak changes were observed within 30 min of drug injection. Cytophotometric studies have appeared to dovetail the biochemical findings. Only a marginal decrease was observed after injection of GABA in all nuclei, while muscimol induced a very conspicuous decrease of BuChE. On the contrary, intracerebroventricularly administered picrotoxin markedly increased the levels of BuChE activity. Thus it could be concluded that probably GABA and muscimol along with picrotoxin appear to alter BuChE.

Animals↗

PubMed1986

The occurrence of gamma-aminobutyric acid (GABA)-containing cells in cultures of retinas from the human fetus.

gamma-Aminobutyric acid (GABA) immunoreactivity is demonstrated by the indirect immunofluorescence technique in a small population of retinal neurons cultured from human fetuses. Positive staining was restricted to a few cells and could be observed as soon as the cells became attached to the substrate (within 5 hr). It is therefore concluded that the GABA-positive cells are determined prenatally. The GABA-positive cells grow processes during development in culture and remain constant in numbers. These cells have a different morphology from either GFAP-positive cells or serotonin-accumulating cells. It is suggested that the GABA-positive cells in culture are probably amacrine neurones. Cultures of human retinal dissociates may therefore provide an alternative means of studying specific cell types should a constant supply of living human retinas be difficult to obtain.

Cells, Cultured↗

PubMed2005

Receptors and sites of synthesis and storage of gamma-aminobutyric acid in human pituitary glands and in growth hormone adenomas.

gamma-Aminobutyric acid (GABA) is an important regulatory factor of pituitary gland function, which in addition to hypothalamic neurons, can be derived from intrapituitary sources, ie, growth hormone (GH) cells of rat and monkey. We report that human pituitary glands also express 2 isoforms of the GABA-synthesizing enzyme glutamate decarboxylase (GAD 65; GAD 67), the vesicular GABA transporter (VGAT), and multiple subunits of GABA (A, B, and C) receptors. GABA production and storage occurs in GH cells, as demonstrated by cellular colocalization of immunoreactive GAD and VGAT in GH cells and by reverse transcription-polymerase chain reaction analysis of laser capture-microdissected immunostained GH cells. It is interesting that human pituitary GH adenomas share expression of VGAT and GABA receptors with normal pituitary glands but lack GAD 65. We propose that GABA, synthesized by GH cells, might act as a paracrine or autocrine regulating factor in the human pituitary gland and in human GH adenoma. Because many drugs interfere with GABA function, the identification of GABA system components might have clinical implications.

Adenoma↗

PubMed1991

Comparative studies on the anticonvulsant activity of lipophilic derivatives of gamma-aminobutyric acid and 2-pyrrolidinone in mice.

Anticonvulsant activity, degradation into gamma-aminobutyric acid (GABA), and concentration in brain of 1-dodecanoyl-2-pyrrolidinone (I), a lipophilic derivative of a lactam of GABA, were compared with those of N-dodecanoyl GABA (II) and 1-dodecyl-2-pyrrolidinone (III) to get information about their pharmacological mechanisms. Compounds I and II degraded into GABA in mouse liver homogenate, gradually into GABA in brain homogenate and more slowly in plasma. Compound III had no degradation in the biological media. The derivatives administered intraperitoneally had dose-dependent anticonvulsant activity on picrotoxin-induced seizure in mice. Their anticonvulsant activities were changed by the time intervals between pretreatment of derivatives and administration of picrotoxin. Compounds II and III showed anticonvulsant activity on pentylenetetrazole-induced seizure and a prolonged sleeping time induced by sodium pentobarbital in mice. However, these three derivatives never significantly increased the GABA level in mouse brain after intraperitoneal administration compared to the endogenous GABA level. They were detected as intact derivatives in the brain. In the previous report, we demonstrated the anticonvulsant activity of sodium dodecanoate. These results suggested that the dodecyl chain of derivatives may be important for their anticonvulsant activities and I does not act as GABA via prodrug.

Animals↗