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PubMed1977

Specific and sensitive method for the determination of gamma-aminobutyric acid using gas chromatography with electron-capture or mass fragmentographic detection.

A gas chromatographic method for the determination of gamma-aminobutyric acid (GABA) in brain tissue is described. After microwave fixation, the brains were dissected and homogenized in 0.1 N formic acid; delta-amino-n-valeric acid (AVA), a homologue of GABA, was then added as an internal standard. After centrifugation, aliquots of the supernatant were treated with cation-exchange paper to adsorb the amino acids. The eluates of this paper were dried and the residues subjected to reaction with trifluoroacetic anhydride and hexafluoroisopropanol. After removal of the derivatization reagents by evaporation, the residues were dissolved in ethyl acetate and an aliquot was analysed by gas chromatography with electron-capture or mass fragmentographic detection. Quantitation can be carried out by either peak-height or peak-area measurements. The specificity of this method has been demonstrated with brain tissue by simultaneous mass fragmentographic analysis. The sensitivity is comparable to that of mass fragmentographic methods and is in the femtomole range. The method is simple and readily automated.

Aminobutyrates↗
PubMed1987

gamma-Aminobutyric acid antagonist blocks baroreceptor-activated inhibition of neurosecretory cells in the hypothalamic paraventricular nucleus of rats.

The effects of gamma-aminobutyric acid (GABA) antagonists on baroreceptor-activated inhibition of neurosecretory cells in the paraventricular nucleus (PVN) were examined in urethane-chloralose anesthetized rats. In 11 neurosecretory cells which were inhibited by baroreceptor activation induced by intravenous application of phenylephrine, microiontophoretically applied bicuculline and/or picrotoxin blocked the inhibition (n = 9) completely or partially, whereas strychnine (n = 4) did not. The results suggest that GABA is, at least in part, involved in the baroreceptor-activated inhibition of PVN neurosecretory cells.

Action Potentials↗
PubMed1988

Melatonin enhancement of [3H]-gamma-aminobutyric acid and [3H]muscimol binding in rat brain.

The pineal hormone, melatonin, enhanced the sodium-independent binding of [3H]-gamma-aminobutyric acid ([3H]GABA) and [3H]muscimol in the rat cerebral cortex in vitro. This effect was augmented by preincubation of synaptic membranes with melatonin but was abolished by preincubation with Triton X-100. Saturation binding studies using [3H]GABA (2.5 to 1000 nM) indicated that the melatonin-induced enhancement of binding is due to an increase in low-affinity GABAA binding sites. These findings suggest that the central effects of melatonin involve modulation of GABAergic function.

Animals↗
PubMed1990

The entopeduncular nucleus regulates muscle tone in genetically spastic rats: role of substance P and gamma-aminobutyric acid.

Microinjections of the substance P (SP) antagonist (D-pro2,D-phe7,D-trp9)-SP, or the gamma-aminobutyric acid (GABA) agonist, muscimol, into the entopeduncular nucleus reduced muscle tone in genetically spastic rats in a dose- and time-dependent manner. Similar injections into the ventral thalamus, zona incerta or amygdala had no effect on muscle tone. The muscle relaxant effect of (D-pro2,D-phe7,D-trp9)-SP injected into the entopeduncular nucleus was blocked by co-injections of SP, and that of muscimol by the GABAA antagonist, bicuculline methiodide. These results suggest that SP- and GABA-dependent mechanisms in the entopeduncular nucleus mediate regulation of the muscle tone.

Animals↗
PubMed1980

Influence of gamma-aminobutyric acid on lordosis behavior and dopamine activity in estrogen primed spayed female rats.

In the first experiment the role of gamma-aminobutyric acid (GABA) in the display of lordosis behavior was examined in septal-lesioned and sham-operated ovariectomized rats. Following estradiol benzoate (EB) priming, septal-lesioned rats were tested for lordosis behavior before and after bilateral infusion of picrotoxin or saline directly into the substantia nigra (SN). Sham animals were given the same behavioral tests but received intranigral infusion of either hydrazinopropionic acid (HPA) or saline. Picrotoxin, which blocks GABA receptors, was effective in suppressing the high levels of lordosis behavior seen in the EB-primed septal-lesioned female rat 30 min after infusion, but not at 120 min. Conversely, HPA, which elevates endogenous GABA levels, was effective in facilitating lordosis behavior in sham-operated rats treated with EB only. The lordosis quotient was moderately increased 30 min after HPA infusion, reached high levels at 120 min, and returned to low levels by 360 min post-infusion, demonstating the reversibility of the drug effect. Saline infusions in lesioned and sham-operated controls were without effect. In the second experiment sepal-lesioned and sham-operated rats were primed with EB and infused with the drugs as in the first experiment, but were sacrificed at the time the macimal behavioral effect had been observed in the first experiment. Tyrosine hydroxylase (TH) activity and dopamine (DA) and homovanillic acid (HVA) levels were measured. No effect on TH activity was found. However, sham-operated rats receiving HPA infusions had lower DA and HVA levels compared to those of saline-injected controls, and septal-lesioned rats receiving picrotoxin infusions had higher DA and HVA levels than those of lesioned saline-injected controls. Septal-lesioned saline-infused rats also showed decreased DA and HVA levels relative to sham-operated saline-infused animals. These results support the concept of a GABA inhibitory neuronal feedback system which modulates DA turnover and perhaps plays a critical role in the neural control of lordosis behavior.

Animals↗
PubMed1985

The action of inhibitory neurotransmitters, gamma-aminobutyric acid and glycine may distinguish between the area centralis and the peripheral retina in cats.

The effects of iontophoretically applied gamma-aminobutyric acid (GABA) and glycine, and of their antagonists, bicuculline and strychnine, were compared between ganglion cells from the central and peripheral retinae of optically intact eyes in barbiturate-anaesthetised cats. The visual response of on-cells was inhibited by GABA and enhanced by bicuculline. The visual response of off-cells was inhibited by glycine and enhanced by strychnine. The sensitivity of cells to the transmitters was lower in the peripheral retina than in the area centralis, whilst the sensitivity to the antagonists was similar in both regions of the retina. Cells from the area centralis were inhibited by either GABA or glycine, but never both. Cells from the periphery were less selective and were inhibited by both transmitters.

Animals↗
PubMed1993

Relation of exocytotic release of gamma-aminobutyric acid to Ca2+ entry through Ca2+ channels or by reversal of the Na+/Ca2+ exchanger in synaptosomes.

The specific inhibitor of the gamma-aminobutyric acid (GABA) carrier, NNC-711, (1-[(2-diphenylmethylene)amino]oxyethyl)- 1,2,5,6-tetrahydro-3-pyridine-carboxylic acid hydrochloride, blocks the Ca(2+)-independent release of [3H]GABA from rat brain synaptosomes induced by 50 mM K+ depolarization. Thus, in the presence of this inhibitor, it was possible to study the Ca(2+)-dependent release of [3H]GABA in the total absence of carrier-mediated release. Reversal of the Na+/Ca2+ exchanger was used to increase the intracellular free Ca2+ concentration ([Ca2+]i) to test whether an increase in [Ca2+]i alone is sufficient to induce exocytosis in the absence of depolarization. We found that the [Ca2+]i may rise to values above 400 nM, as a result of Na+/Ca2+ exchange, without inducing release of [3H]GABA, but subsequent K+ depolarization immediately induced [3H]GABA release. Thus, a rise of only a few nanomolar Ca2+ in the cytoplasm induced by 50 mM K+ depolarization, after loading the synaptosomes with Ca2+ by Na+/Ca2+ exchange, induced exocytotic [3H]GABA release, whereas the rise in cytoplasmic [Ca2+] caused by reversal of the Na+/Ca2+ exchanger was insufficient to induce exocytosis, although the value for [Ca2+]i attained was higher than that required for exocytosis induced by K+ depolarization. The voltage-dependent Ca2+ entry due to K+ depolarization, after maximal Ca2+ loading of the synaptosomes by Na+/Ca2+ exchange, and the consequent [3H]GABA release could be blocked by 50 microM verapamil. Although preloading the synaptosomes with Ca2+ by Na+/Ca2+ exchange did not cause [3H]GABA release under any conditions studied, the rise in cytoplasmic [Ca2+] due to Na+/Ca2+ exchange increased the sensitivity to external Ca2+ of the exocytotic release of [3H]GABA induced by subsequent K+ depolarization. Thus, our results show that the vesicular release of [3H]GABA is rather insensitive to bulk cytoplasmic [Ca2+] and are compatible with the view that GABA exocytosis is triggered very effectively by Ca2+ entry through Ca2+ channels near the active zones.

Animals↗
PubMed1995

Initial observations on effect of vigabatrin on in vivo 1H spectroscopic measurements of gamma-aminobutyric acid, glutamate, and glutamine in human brain.

Recent developments involving 1H nuclear magnetic resonance (NMR) spectroscopic editing techniques have allowed noninvasive measurements of gamma-aminobutyric acid (GABA) in human cerebrum. The additional information gained from GABA and macromolecule measurements permitted more precise glutamate (Glu) and glutamine (Gln) measurements. Occipital lobe GABA in 10 nonepileptic, healthy subjects was 1.0 mumol/g brain [95% confidence interval (CI) 0.9-1.1]. Vigabatrin (VGB) is a safe and effective antiepileptic drug (AED) that irreversibly inhibits neuronal and glial GABA-transaminase. GABA levels were increased in all patients treated with VGB. With a standard dose of 3-6 g/day, GABA levels were 2.6 mumol/g (95% CI 2.3-2.8). Mean occipital GABA level measured in epileptic patients not receiving VGB was 0.9 mumol/g (95% CI 0.7-1.1). Gln was increased by 1.9 mumol/g and Glu was decreased by 0.8 mumol/g in patients receiving VGB as compared with patients receiving standard medications alone.

Adult↗
PubMed2006

Hydroxy-1,2,5-oxadiazolyl moiety as bioisoster of the carboxy function. Synthesis, ionization constants, and pharmacological characterization of gamma-aminobutyric acid (GABA) related compounds.

Three 4-substituted 1,2,5-oxadiazol-3-ols containing aminoalkyl substituents (analogues and homologues of gamma-aminobutyric acid (GABA)) were synthesized to investigate the hydroxy-1,2,5-oxadiazolyl moiety as a bioisoster for a carboxyl group at GABA receptors. The pK(a) values of the target compounds were close to those of GABA. At GABA(A) receptors of cultured cerebral cortical neurons, weak agonist and partial agonist profiles were identified, demonstrating the 4-hydroxy-1,2,5-oxadiazol-3-yl unit to be a nonclassical carboxyl group bioisoster.

Animals↗
PubMed2000

Percentage incidence of gamma-aminobutyric acid neurons in the claustrum of the rabbit and comparison with the cortex and putamen.

We describe the incidence of gamma-aminobutyric acid (GABA)ergic neurons after post-embedding immunocytochemistry on semithin sections of the claustrum, putamen and lateral, dorsal and medial cortical areas. Twelve percent of the neurons counted in the claustrum of 11 rabbits were GABAergic. This incidence was significantly higher in the dorsal halves of both the insular and endopiriform claustra than in the ventral (13 vs. 10%). The incidence of GABAergic cells was 4% in the putamen, 14% in the insular cortex, 15% in areas 17 and 18 and 13% in area 29d. Thus, our results indicate that in contrast to the putamen the incidence of GABAergic cells was similar in the claustrum and cortical areas. We interpret this in the light of the pallial origin of the claustrum, which has recently been substantiated.

Animals↗
PubMed2001

Cannabinoid receptor agonist WIN 55,212-2 inhibits rat cortical dialysate gamma-aminobutyric acid levels.

The effects of the cannabinoid receptor agonist WIN 55,212-2 (0.1-5 mg/kg i.p.) on endogenous extracellular gamma-aminobutyric acid (GABA) levels in the cerebral cortex of the awake rat was investigated by using microdialysis. WIN 55,212-2 (1 and 5 mg/kg i.p.) was associated with a concentration-dependent decrease in dialysate GABA levels (-16% +/- 4% and -26% +/- 4% of basal values, respectively). The WIN 55,212-2 (5 mg/kg i.p.) induced-inhibition was counteracted by a dose (0.1 mg/kg i.p.) of the CB(1) receptor antagonist SR141716A, which by itself was without effect on cortical GABA levels. These findings suggest that cannabinoids decrease cortical GABA levels in vivo, an action that might underlie some of the cognitive and behavioral effects of acute exposure to marijuana.

Animals↗
PubMed1993

Gamma-aminobutyric acid mediation of the inhibitory effect of endogenous opioids on the arginine vasopressin and oxytocin responses to nicotine from cigarette smoking.

Previous studies have demonstrated that naloxone exerts positive effects on the responsiveness of arginine vasopressin (AVP) and oxytocin (OT) to nicotine, suggesting inhibitory actions of endogenous opioids. The present study was designed to determine whether a gamma-aminobutyric acid (GABA)ergic pathway is involved in the regulation of naloxone-sensitive endogenous opioid action. AVP and OT secretory patterns after (two nonfilter) cigarette smoking were examined in seven normal male subjects with (experimental test) and without (control test) concomitant treatment with naloxone (4 mg in an intravenous bolus plus 6 mg infused over 2 hours), the GABAergic agent sodium valproate (600 mg in three divided doses orally), or the combination of naloxone and sodium valproate. Cigarette smoking increased by 2.4-fold (peak v baseline) the plasma concentrations of AVP without modifying OT levels. In the presence of naloxone, plasma AVP and OT levels in response to nicotine were significantly higher than those in the control test. In the naloxone plus nicotine test, AVP levels increased 4.2-fold (peak v baseline) and OT concentrations increased 1.6-fold (peak v baseline). Pretreatment with sodium valproate changed neither AVP nor OT secretory patterns during the cigarette-smoking test. In contrast, sodium valproate abolished the facilitating effect of naloxone on both AVP and OT responses to nicotine. In the sodium valproate plus naloxone plus nicotine test, plasma AVP and OT levels were not significantly higher than those obtained during the nicotine test. These data indicate a GABAergic mediation of the inhibitory modulation by endogenous opioids of the AVP and OT responses to nicotine.

Adult↗
PubMed1996

Involvement of protein kinase C in gamma-aminobutyric acid release from Xenopus oocytes injected with rat brain mRNA.

Involvement of protein kinase C (PKC) in the release of gamma-aminobutyric acid (GABA) was examined in Xenopus laevis oocytes injected with mRNA from rat cerebellum, as compared with findings in slices of rat cerebellum. The mRNA-injected oocytes preloaded with [3H]GABA showed spontaneous release of [3H]GABA, approximately 0.5% of GABA content per 1 min. Stimulation with either Ca2+ ionophore (A23187) or a high K+ concentration increased the release of [3H]GABA from slices of rat deep cerebellar nucleus and mRNA-injected oocytes but not from noninjected and water-injected oocytes. 12-O-Tetradecanoylphorbol 13-acetate (10-300 nM) but not 4alpha-phorbol 12,13-didecanoate (300 nM) potentiated the A23187-stimulated release of [3H]GABA from slices and from mRNA-injected oocytes, in a concentration-dependent manner. Thus, machinery associated with release processes of GABA can be expressed in oocytes by injecting rat cerebellar mRNA, and PKC participates in GABA release from the functionally expressed GABAergic nerve terminals.

Animals↗
PubMed2003

Evidence of association between gamma-aminobutyric acid type A receptor genes located on 5q34 and female patients with mood disorders.

Pharmacological evidence suggests the involvement of gamma-aminobutyric acid (GABA) perturbation in the etiology of mood disorders. A linkage study has detected chromosomal area 5q34, where GABA type A (GABA(A)) receptor subunit genes are mapped, as a susceptibility region for mood disorders, making these genes compelling candidates for such diseases. Our prior quantitative trait loci (QTL) analysis of mouse depression models identified a QTL on mouse chromosome 11, a genomic region whose human synteny includes 5q34. This further supports a contribution from GABA(A) receptors to a predisposition towards mood disorder. In the present study, we examined GABA(A) receptor alpha1 (GABRA1), alpha6 (GABRA6) and gamma2 (GABRG2) subunit genes on 5q34. Polymorphisms on GABRA1 and GABRA6 genes displayed significant associations with mood disorders in female patients. These data offer genetic support for a role of GABA(A) receptor genes in susceptibility to mood disorders.

Adult↗
PubMed1986

Comparison of the effect of gamma-aminobutyric acid and its derivative baclofen on the activity of Purkinje cells of frog cerebellum in vitro.

The inhibitory effect of gamma-aminobutyric acid (GABA) and its synthetic derivative baclofen were compared in frog cerebellum in vitro. Baclofen inhibited synaptic transmission from parallel fibres to the Purkinje cells in EC50 concentrations approximately 200-fold lower than for GABA. In addition to its inhibitory effect, GABA induced temporary facilitation of responses in the dendrite zone by a mechanism dependent on the presence of a normal Cl- concentration; the inhibitory phase was only partly sensitive to reduction of the Cl- concentration in the medium and to the administration of picrotoxin. The action of baclofen, which was unaffected by these treatments, requires an intact catecholamine and serotonin pool, since it is ineffective in reserpine-treated animals. Both substances also influence the excitability of parallel fibres. In solutions with a high Mg2+ and a low Ca2+ concentrations GABA inhibits the spontaneous activity of Purkinje cells by acting on the postsynaptic membrane of the soma and the primary dendrites. The effect of baclofen is evidently the outcome of inhibition of transmitter release from presynaptic endings.

Action Potentials↗
PubMed2007

Antihypertensive and natriuretic effects of less-sodium soy sauce containing gamma-aminobutyric acid in spontaneously hypertensive rats.

We investigated the mechanism of the antihypertensive effect of less-sodium soy sauce containing gamma-aminobutyric acid (GABA) in spontaneously hypertensive rats (SHRs). When SHRs were given a diet with less-sodium soy sauce containing GABA (GABA-rich soy sauce group) for 6 weeks, the systolic blood pressure decreased as compared with that in rats fed diets with less-sodium soy sauce or a solution of salt. Renal sympathetic nerve activity (RSNA) and positive Na balance were reduced, and the urinary Na excretion tended to increase in the GABA-rich soy sauce group. Vascular hypertrophy of the thoracic aorta and the coronary and renal interlobular arteries tended to reduce in the GABA-rich soy sauce group. These results suggest that inhibition of Na retention by natriuresis, as a result of inhibition of RSNA by the GABA in the soy sauce contributed to the antihypertensive effect of GABA in the SHRs. Intake of less-sodium soy sauce containing GABA might help to reduce overall cardiovascular risk.

Administration, Oral↗
PubMed1992

[Immunohistochemical distribution and fine localization of the gamma-aminobutyric acid in the organ of Corti of normal guinea pigs].

This paper presents the distribution and fine localization of the gamma-aminobutyric acid (GABA) in the Corti's organ of normal guinea pigs by using immunohistochemical technique (ABC-GDN method) and immunoelectron microscopy. GABA-IR was found in axons of efferent neurons in all turns of the cochlear spiral, but no positive endings may be found in the apical. The positive immunoreactive products were seen in the efferent components, including inner spiral bundle, tunnel spiral bundle, tunnel-crossing fibers, and large nerve endings on outer hair cell bases. Some of the GABA-IR negative outer hair cells could be seen between the positive endings. One GABA-IR positive nerve fiber could form synapse with six or seven outer hair cell bases. The GABA-IR positive efferent endings, negative efferent endings and negative afferent endings could be seen on the out hair cell bases with transmission electronic microscope. The GABA-IR positive efferent endings and negative afferent endings could form the neuraxon-neurodendron synapse on the inner hair cells bases. These morphological distribution suggests that the GABA may be one of the cochlear efferent neurotransmitter or modulator.

Animals↗