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PubMedDate not supplied

Cerebrospinal fluid gamma-aminobutyric acid levels in children with different types of epilepsy: effect of anticonvulsant treatment.

The mean gamma-aminobutyric acid (GABA) level in lumbar CSF of 31 children with epilepsy was not significantly different from that of 41 age-matched controls. However, when the epileptic children were subdivided into untreated patients and patients treated with antiepileptic drugs, the medication-free subgroup had a significantly lower mean CSF GABA level than nonepileptic children. Patients controlled by anticonvulsant therapy had significantly higher CSF GABA levels than untreated epileptic patients. A more detailed analysis of the children taking antiepileptic medication indicated that the only drug that significantly increased GABA in CSF was valproic acid. Analysis of CSF data with respect to the seizure type of the patients showed that, compared with controls, significantly reduced average GABA levels were present in children with infantile spasms (mostly untreated) and unmedicated generalized tonic-clonic seizures, whereas treated children with generalized tonic-clonic seizures and patients with partial epilepsy (mostly treated) did not significantly differ from controls. The data provide further evidence that impairment of the central GABA system may be involved in human epilepsy.

Adolescent↗
PubMed1986

Conversion of 4-aminobutyraldehyde to gamma-aminobutyric acid in striatum treated with semicarbazide and kainic acid.

4-Aminobutyraldehyde (ABAL) has been shown to cross the blood-brain barrier and to be converted rapidly to gamma-aminobutyric acid (GABA) in various regions of the brain. In this paper, the formation of GABA from ABAL was studied with striatum that had suffered a lesion to GABA synthesis via glutamic acid decarboxylase (GAD). The GABA formation from ABAL was invariably observed in striatum in which GAD was severely inhibited by semicarbazide or kainic acid. Thus, this is another pathway for GABA formation.

Aldehydes↗
PubMed1992

Molecular heterogeneity of the gamma-aminobutyric acid (GABA) transport system. Cloning of two novel high affinity GABA transporters from rat brain.

cDNA clones encoding two novel gamma-aminobutyric acid (GABA) transporters (designated GAT-2 and GAT-3) have been isolated from rat brain, and their functional properties have been examined in mammalian cells. The transporters display high affinity for GABA (Km approximately 10 microM) and exhibit pharmacological properties distinct from the previously cloned neuronal GABA transporter (GAT-1). Both transporters require sodium and chloride for transport activity. The nucleotide sequences of GAT-2 and GAT-3 predict proteins of 602 and 627 amino acids, respectively, which can be modeled with 12 transmembrane domains, similar to the topology proposed for other cloned neurotransmitter transporters. Localization studies indicate that both transporters are present in brain and retina, while GAT-2 is also present in peripheral tissues. The cloning of these transporter genes from rat brain reveals previously undescribed heterogeneity in GABA transporters.

Amino Acid Sequence↗
PubMed1987

Modulation of gamma-aminobutyric acid uptake of rat brain synaptosomes by thyroid hormones.

The effects of thyroid hormones on gamma-aminobutyric acid (GABA) uptake were compared in homogenates and purified synaptosomes from rat cerebral cortex. L-triiodothyronine (T3) and L-thyroxine (T4), but not reverse T3(rT3), blocked GABA uptake in homogenates when hormone and labeled GABA were added to the system simultaneously. Similar effects were obtained when homogenates were preincubated with hormone and washed to remove free hormone before addition of GABA. A competitive inhibitor of neuronal GABA uptake, diaminobutyric acid (DABA), blocked GABA uptake when added with GABA, but not after preincubation and washing. In purified synaptosomes, T3, T4, and rT3 blocked GABA uptake when added simultaneously with GABA and also after preincubation and washing before addition of GABA, thus indicating that binding of hormones had occurred. Other experiments suggested that hormone binding was not at the GABA recognition site and that the effect of T4 was not dependent on conversion to T3.

Animals↗
PubMed1985

Aminobutyric acid greatly increases the in vivo extracellular taurine in the rat hippocampus.

The effects of gamma-aminobutyric acid (GABA) on the extracellular levels of taurine and on excitability in the dentate gyrus were studied in anesthetized rats by the dialytrode technique. The dentate gyrus was perfused by means of a dialytrode with Krebs-Ringer-bicarbonate or GABA solutions. Amino acid contents in perfusates and dentate field potentials evoked by electrical stimulation of the perforant pathway were evaluated. GABA drastically elevated the levels of extracellular taurine in a dose-dependent manner, decreasing the amplitude of the population spike. This result indicates that GABA stimulates taurine release, probably by a counter-transport process. It is suggested that in physiological conditions an increase in extracellular taurine may be produced by synaptically released GABA.

Animals↗
PubMed1979

[3H]gamma-Aminobutyric acid uptake into neuroglial cells of rat superior cervical sympathetic ganglia.

1. The influx of [3H]gamma-aminobutyric acid ([3H]GABA) into isolated rat superior cervical ganglia has been measured by radioassay, supplemented by autoradiography. Ganglia were incubated in oxygenated Krebs solution at 25 degrees C, containing 10 microM-amino-oxyacetic acid. Under these conditions more than 95% of accumulated tritium was unmetabolized [3H]GABA. 2. Ganglionic radioactivity increased linearly with incubation time, to yield an intracellular fluid/extracellular fluid concentration ratio (Ci/Co) of about 200 after 6 hr in 0.5 microM-external [3H]GABA. 3. Uptake showed saturation with an apparent transport constant (KT) of 6.8 microM and maximum influx velocity (Jmaxi) of 7 mumole 1. cell fluid-1- min-1. 4. The influx rate at Co = 0.5 microM was unaltered by raising intracellular GABA from 0.2 to 1 mM. 5. Influx velocity increased with temperature (5--35 degrees C) in a monotonic manner with an apparent activation energy of 14 kcal mole-1. 6. Concentrative uptake was depressed by reducing external [Na+] with ouabain, by raising [K+]o above 20 mM, or by removing external Cl-. Uptake was not particularly sensitive to Ca2+ or Mg2+ ions. 7. Utake of [3H]GABA (0.5 microM) was inhibited by beta-guanidinopropionic acid (apparent KI, 28 microM), beta-alanine (KI, 55 microM), gamma-amino-beta-hydroxybutyric acid (KI, 220 microM), beta-amino-n-butyric acid (KI, 708 microM), 3-aminopropanesulphonic acid (KI, 832 microM) and taurine (KI greater than 1 mM). Uptake was not depressed by 1 mM-glycine, alpha-alanine, leucine, serine, methionine or alpha-amino-iso-butyric acid. 8. Radioactively labelled methionine, leucine, glycine, serine, beta-alanine and taurine (concentrations less than or equal to 5 microM) were also taken up by ganglia. Of these, only uptake of beta-alanine and taurine were significantly depressed by 1 mM-GABA. 9. Autoradiographs confirmed that [3H]GABA and [3H] beta-alanine were taken up predominantly into extraneuronal sites (presumed to be neuroglial cells). Methionine, leucine, glycine and serine showed preferential accumulation in neurones. Neuronal uptake of leucine was not prevented by inhibiting protein synthesis. 10. Calculations of net fluxes from unidirectional tracer fluxes suggest that the sympathetic glial cells are capable of promoting net uptake of GABA at external concentrations above 1 microM.

Amino Acids↗
PubMed1992

[Study on variation of plasma gamma-aminobutyric acid concentration in rat model of hepatic encephalopathy due to fulminant hepatic failure].

The plasma gamma-aminobutyric acid (GABA) concentration was measured by a radio-receptor assay in rat model of hepatic encephalopathy due to fulminant hepatic failure (FHF) induced by intraperitoneal injection of D-galactosamine (GalN). The results showed that, in FHF group, the plasma GABA increased parallelly with the degree of hepatic encephalopathy after GalN i.p. (r = 0.944, P less than 0.05). In about 48 h, mean plasma GABA concentration was elevated nearly 8-fold. These findings suggest that, in liver failure, elevated plasma GABA concentration may play a role in the pathogenesis of hepatic encephalopathy.

Animals↗
PubMed1988

Light- and electron-microscopic study of gamma-aminobutyric-acid-like immunoreactivity in the guinea pig organ of Corti.

With light and electron microscopy, gamma-aminobutyric-acid (GABA)-like immunoreactivity was examined in the guinea pig organ of Corti. In whole-mount preparations, although GABA-like immunoreactivity was present within efferent components in all turns of the cochlea, it was more intense apically. At the ultrastructural level, GABA-like immunoreactivity was clearly restricted to the efferent system, appearing in axons of the inner and tunnel spiral bundles, in axons crossing the tunnel of Corti, and in terminals filled with numerous labeled vesicles synapsing on outer hair cells.

Animals↗
PubMed1985

A specific and sensitive determination of gamma aminobutyric acid in CSF and brain tissue by gas chromatography-mass spectrometry.

The determination of gamma-aminobutyric acid (GABA) in cerebrospinal fluid and brain extracts is described. Its heptafluorobutyryl-isobutanol derivative was measured both by electron impact and chemical ionization mass fragmentography using GABA-d6 as internal standard. The derivatization product is stable for several days. The method is sensitive (1 ng absolute in cerebrospinal fluid and 30 pg in standard GABA solutions) and specific, when chemical ionization mode is applied. Normal values of GABA are in rat brain extracts (1.40 +/- 0.32 mumol/g fresh weight) and human CSF (18.3 +/- 10.0 ng/ml).

Animals↗
PubMed1985

Presence of gamma-aminobutyric acid and its specific receptor binding sites in the human term placenta.

The concentration of gamma-aminobutyric acid (GABA), the activity of glutamate decarboxylase (GAD), and the presence of specific GABA receptor binding sites have been examined in human term placentas. The estimated values of GABA concentration and GAD activity in the placenta were about 50 nmol/g tissue and 1.1 nmol/mg protein/h, respectively. A remarkable density of high-affinity and specific GABA binding sites has also been demonstrated in membranes of the human term placenta. These binding sites showed the properties of a GABAA receptor. The present findings suggest a possible role of GABA in the function of human placenta.

Female↗
PubMed1983

4-Aminobutyraldehyde as a precursor convertible to gamma-aminobutyric acid in vivo.

It was found that 4-aminobutyraldehyde (ABAL) is a precursor convertible to gamma-aminobutyric acid (GABA) in vivo. [2,3-3H]ABAL was synthesized from [2,3-3H]putrescine. After the subcutaneous administration of [3H]ABAL at the dose of 1 mumol/g body weight, [3H]GABA was produced in the mouse brain in an amount of about 350 nmol/g brain in 10 min. After oral administration of [3H]ABAL at the dose of 2 mumol/g body weight, [3H]GABA was also produced in the brain in an amount of about 530 nmol/g brain in 30 min. It seems that peripherally administered ABAL penetrates the blood-brain barrier into the central nervous system and is rapidly metabolized to GABA in the brain.

Aldehydes↗
PubMed1983

Effects of gamma-aminobutyric acid on insulin, glucagon, and somatostatin release from isolated perfused dog pancreas.

The effects of gamma-aminobutyric acid (GABA) on the secretion of insulin, glucagon, and somatostatin were studied in the isolated dog pancreas. Insulin secretion was inhibited in a dose-related fashion for 10 min or more by as little as 1 microM GABA. A prompt but small and transitory rise in somatostatin secretion, lasting only 1 min, occurred at GABA concentrations of 10 and 100 microM, levels that exert inhibitory effects on nervous tissue. Bicuculline, a GABA antagonist, inhibited insulin secretion and did not antagonize GABA-mediated insulin inhibition. The results suggest that GABA in concentrations that are known to exist in islet tissue can influence the secretion of islet hormones.

Animals↗
PubMed1989

Chelation of endogenous membrane calcium inhibits gamma-aminobutyric acid uptake in synaptosomes.

In a previous work, we have demonstrated that calcium chelators induce the release of gamma-aminobutyric acid (GABA) from synaptosomes in a Na+ -dependent manner and that this release is blocked by cations such as Mg2+, La3+, and ruthenium red. In the present study, we show that treatment of synaptosomes with 0.1 mM EGTA in the absence of both Ca2+ and Mg2+ inhibits the sodium-dependent high-affinity uptake of [3H]GABA by about 50%. This inhibition increased to about 65% with 1.5 mM EGTA, and it was completely prevented by an excess of Ca2+ or by 1.2 mM Mg2+. In contrast, when EDTA was used as a chelator, Mg2+ was unable to reverse the inhibition. The inhibitory effect of 0.1 mM EGTA was also prevented by 250 microM La3+ or by 20 microM ruthenium red. In the absence of chelators and the presence of Ca2+ and Mg2+, 50 microM and 200 microM La3+ inhibited GABA uptake by about 20 and 50%, respectively, whereas 20 microM ruthenium red produced a nonsignificant 25% inhibition and nifedipine was without effect. It is concluded that the membrane-surface negative charges, probably those of the sialic acid molecules that have been implicated in the functioning of the GABA carrier, must be neutralized by endogenous Ca2+ or by another cation in order to permit the adequate function of the transporter. The inhibition by La3+ in the absence of the chelators could be explained by a binding of this cation to the Na+ sites on the GABA carrier.

Animals↗
PubMed1981

Role of central nervous system-derived or circulating gamma-aminobutyric acid on prolactin secretion in the rat.

To investigate the respective role in PRL secretion of gamma-aminobutyric acid (GABA), either derived from the central nervous system or circulating in plasma, experiments were performed using ethanolamine-O-sulfate (EOS), a specific inhibitor of GABA catabolism. Intracerebroventricular injection of EOS (2 mg/kg) induced in unanesthetized male rats 2-8 h post injection a clear-cut rise in hypothalamic, anterior pituitary (AP), and plasma GABA concentrations. Rises in GABA titers occurred earlier in the hypothalamus and AP (2 h) than in the plasma (4 h). Concomitant to alterations of GABA, there was a striking lowering of plasma PRL evident at 2 h and still present 24 h after EOS administration. In contrast, systemic administration of graded doses of EOS (200-400 mg/kg, iv) did not induce significant changes in plasma GABA concentrations 4 h post injection; only the 600 mg/kg dose of EOS increased GABA concentrations 4 h post injection in the hypothalamo-AP system and decreased plasma PRL concentrations. Finally, in hypophysectomized rats bearing ecotopic pituitaries, despite the occurrence of rises in the hypothalamic GABA after intracerebroventricular or systemic (600 mg/kg) administration of EOS, AP, plasma GABA, and plasma PRL concentrations were not altered. In all these findings indicate that: 1) changes in plasma PRL are best correlated to variations in the amino acid titers occurring in the hypothalamo-AP systems; and 2) circulating GABA does not play a functional role in the control of PRL secretion. Finally, since alterations in blood GABA levels after central or systemic administration of EOS appear to reflect primary changes occurring in the brain concentration of the amino acid, circulating GABA may be a reliable indicator of central nervous system GABAergic function.

Aminobutyrates↗
PubMed1995

[Coriaria lactone on gamma-aminobutyric acid secretion and glutamic acid decarboxylase and its receptor binding in rat].

The effects of coriaria lactone (CL) on gamma-aminobutyric acid (GABA) secretion, glutamic acid decarboxylase (GAD) activity and glutamate (Glu) receptor binding were studied by using cultured neurons, P2 component and synaptic membranes from rat cerebral cortex. It was found that GABA secretion was depressed by CL, the depression rate was 8.3%, 10.6%, 14.5% at 12h 24h 48h respectively. GAD activity was depressed by CL in concentration of 0.15-150 mumol/L. The depression rate was 1.32%, 5.96%, 13.24%, 18.76% respectively. The Glu receptor binding capability was decreased by CL with obvious dose-effect relation in the extent of 2.8-350 mumol/L; the decrease rate was 4.4%, 12.7%, 15.2%, 19.5% respectively. The difference was significant as compared to control (P < 0.01).

Animals↗
PubMed1989

Role of gamma-aminobutyric acid in antipanic drug efficacy.

All effective pharmacologic agents used to treat panic disorder augment gamma-aminobutyric acid (GABA) transmission. Anxiolytics and antidepressants that lack GABA activity are not effective in panic disorder. To test the hypothesis that GABA activity is a component of antipanic drug efficacy, the authors treated nine medication-free panic disorder subjects with oral baclofen (30 mg/day for 4 weeks) in a double-blind, placebo-controlled crossover trial. Baclofen, a selective GABA agonist, was significantly more effective than placebo in reducing the number of panic attacks and scores on the Hamilton anxiety scale, Zung scale, and Katz-R nervousness subscale. The authors discuss possible mechanisms of antipanic drug efficacy.

Anxiety Disorders↗
PubMed2001

Melatonin modulates gamma-aminobutyric acid(A) receptor-mediated currents on isolated carp retinal neurons.

Modulation by melatonin of gamma-aminobutyric acid(A) (GABA(A)) receptor-mediated responses was studied in bipolar and amacrine-like cells acutely isolated from carp retina, using the whole-cell patch-clamp technique. Melatonin of 1 mM accelerated desensitization of the GABA(A) receptors at both bipolar and amacrine-like cells. In addition, 1 mM melatonin hardly changed the GABA(A) receptor-mediated response amplitude of bipolar cells, while it increased or decreased that of amacrine-like cells, depending on the concentration of GABA applied. These modulatory effects, which can not be blocked by luzindole, a melatonin receptor antagonist, may be due to the allosteric action caused by melatonin bound to a site of the GABA(A) receptors.

Animals↗
PubMed1980

Dietary folic acid and the activity of brain cholinergic and gamma-aminobutyric acid (GABA) enzymes.

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.

Acetylcholinesterase↗