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At least 973 records · Page 54Linked to original sources
PubMed1987

gamma-Aminobutyric acid immunoreactivity in brainstem auditory nuclei of the chicken.

Using an antiserum directed against gamma-aminobutyric acid (GABA), the presence of presumed GABAergic neurons is demonstrated in the chicken auditory brainstem nuclei: nucleus laminaris, nucleus angularis, superior olive, and the ventral nuclei of the lateral lemniscus. Nucleus magnocellularis contains no immunopositive neurons but numerous GABA-positive terminals surrounding the cells. Terminal labeling is also present in the other auditory nuclei, though scarcer and not always associated with cell bodies. These data suggest an involvement of GABAergic inhibition in auditory processing in the lower auditory pathway of birds.

Animals↗
PubMed1996

Cromakalim differentially enhances antinociception induced by agonists of alpha(2)adrenoceptors, gamma-aminobutyric acid(B), mu and kappa opioid receptors.

The influence of the ATP-sensitive K+(KATP) channel opener cromakalim on the antinociception induced by agonists of several receptors coupled to pertussis toxin-sensitive G proteins, clonidine (alpha2 adrenoceptor), baclofen (gamma-aminobutyric acid(B) receptor), morphine (mu opioid receptor) and U50,488H (kappa opioid receptor), was evaluated with a tail-flick test in mice. The subcutaneous administration of clonidine (0.12-2 mg/kg), morphine (0.5-16 mg/kg), baclofen (2-16 mg/kg) and U50,488H (2-16 mg/kg) induced a dose-dependent antinociceptive effect. Cromakalim (8-64 microgram/mouse intracerebroventricularly [i.c.v.]) did not change tail-flick latency in control animals but produced a dose-dependent enhancement of the antinociception induced by clonidine and morphine, and shifted their dose-response curves to the left. These effects of cromakalim were antagonized dose dependently by the K(ATP) channel blocker gliquidone (0.1-8 microgram/mouse i.c.v.). On the other hand, cromakalim (16-64 microgram/mouse i.c.v.) did not significantly enhance the antinociception induced by baclofen and U50,488H and did not shift their dose-response curves. These results suggest that opening of the K(ATP) channels plays an important role in the antinociception mediated by alpha(2) adrenoceptors and mu opioid receptors, but not in that induced by gamma-aminobutyric acid(B) and kappa opioid receptors.

Animals↗
PubMed1984

Growth hormone secretion of the neonatal rat pituitaries is stimulated by gamma-aminobutyric acid in vitro.

Growth hormone secretion from pituitaries of neonatal rats was stimulated by gamma-aminobutyric acid (GABA) and the GABA agonist muscimol in vitro. This response to GABA was absent after the 9th postnatal day. The stimulation of growth hormone secretion by GABA was antagonized by bicuculline-methiodide and by picrotoxin. Diazepam stimulated while baclophen had no effect on growth hormone secretion. This stimulatory GABA effect might be related to a certain developmental stage of the pituitary GABA receptors or to the lack of hypothalamic regulatory influence(s) in the newborn.

Aging↗
PubMed1987

Mass fragmentographic determination of gamma-aminobutyric acid and glutamic acid in discrete amygdaloid nuclei of rat brain.

A mass fragmentographic method for the simultaneous quantification of gamma-aminobutyric acid (GABA) and glutamic acid is described. In a convenient one-step reaction, the two amino acids were derivatized with pentafluoropropionic anhydride and pentafluoropropanol. The derivatization products were stable for several days. The technique has been applied to the assay of GABA and Glu in five amygdaloid nuclei of the rat brain. The GABA level was high in the central and medial nuclei, whereas the Glu level was high in the lateral and basal nuclei. The regional distribution of GABA was different from that of Glu within the amygdaloid nuclei.

Amygdala↗
PubMed1988

Putrescine, a source of gamma-aminobutyric acid in the adrenal gland of the rat.

Putrescine is the major source of gamma-aminobutyric acid (GABA) in the rat adrenal gland. Diamine oxidase, and not monoamine oxidase, is essential for GABA formation from putrescine in the adrenal gland. Aminoguanidine, a diamine oxidase inhibitor, decreases the GABA concentration in the adrenal gland by more than 70% after 4 h, and almost to zero in 24 h. Studies using [14C]putrescine confirm that [14C]GABA is the major metabolite of putrescine in the adrenal gland. Inhibition of GABA transaminase by amino-oxyacetic acid does not change the GABA concentration in the adrenal gland, as compared with the brain, where the GABA concentration rises. With aminoguanidine, the turnover time of GABA originating from putrescine in the adrenal gland is 5.6 h, reflecting a slower rate of GABA metabolism compared with the brain. Since GABA in the adrenal gland is almost exclusively derived from putrescine, the role of GABA may relate to the role of putrescine as a growth factor and regulator of cell metabolism.

Adrenal Glands↗
PubMed1983

Enhancement of diazepam and gamma-aminobutyric acid binding by (+)etomidate and pentobarbital.

(+)Etomidate and pentobarbital enhance [3H]diazepam and [3H]gamma-aminobutyric acid [( 3H]GABA) binding to cerebral cortex membranes. Both (+)etomidate and pentobarbital increase the affinity of [3H]diazepam for its binding sites. In contrast, they increase the Bmax of both the high- and low-affinity GABA receptor sites. The enhancement of [3H]diazepam and [3H]GABA by (+)etomidate and pentobarbital is blocked by GABA antagonists. These results indicate that hypnotic drugs such as (+)etomidate and pentobarbital, which are not structurally related, modulate diazepam and GABA binding sites via similar mechanisms.

Animals↗
PubMed1982

Plasma and cerebrospinal fluid gamma-aminobutyric acid in neurological disorders.

In 49 patients with various neurological disorders plasma and CSF gamma-aminobutyric acid (GABA) concentrations were determined by radioreceptor assay. The CSF GABA concentration of 127 +/- 47 pmol/ml (range: 65-275; n = 52) was independent of the age, the sex and the intake of various drugs including benzodiazepines, baclofen and antidepressants. Patients with diverse neurological disorders such as multiple sclerosis, ischaemic strokes, intracranial tumour and polyneuropathies had similar CSF GABA levels. The mean plasma GABA concentration was 309 +/- 79 pmol/ml (range: 179-498; n = 44). The correlation between the GABA concentrations of CSF and plasma was very poor (r = 0.18; n = 44). Therefore plasma GABA is not a suitable indicator for CSF GABA.

Brain Neoplasms↗
PubMed1986

gamma-Aminobutyric acid hyperpolarizes rat hippocampal pyramidal cells through a calcium-dependent potassium conductance.

Application of gamma-aminobutyric acid (GABA) to the dendrites of CA1 pyramidal cells in hippocampal slices produced depolarizing and hyperpolarizing responses. Picrotoxin (50 microM) blocked the depolarizing response of the dendrites to GABA but not the hyperpolarizing responses of the dendrites. The hyperpolarizing response of the cell body to GABA was reduced but not blocked by picrotoxin, suggesting the presence of a complex response at the cell body. The depolarizing response of the dendrites and the hyperpolarizing response of the cell body appeared to be at least partly Cl- dependent as they were respectively increased and decreased in size in low-Cl- artificial cerebrospinal fluid (ACSF), while the hyperpolarizing response of the dendrites was unaffected. The hyperpolarizing response of the dendrites was increased in amplitude in low-K+ ACSF and the extrapolated reversal potential of the response became more negative, suggesting that the response was K+ dependent. The hyperpolarizing response of the dendrites was decreased in size in high-K+ ACSF and could be readily inverted by current injection. The reversal potential became less negative in high-K+ ACSF in a similar manner to that of the slow after-hyperpolarization following a train of spikes, indicating that the response was a K+ conductance. Perfusion of the slice with normal or 0-Ca2+ ACSF containing Cd2+ or Mn2+ blocked synaptic transmission, increased spike duration and blocked the slow phase of the spike after-hyperpolarization (a.h.p.). This latter potential is thought to be mediated by a Ca2+-dependent K+ conductance. Later, the hyperpolarizing response of the dendrites to GABA was blocked without an effect on the other GABA responses. Pressure application of Cd2+ (0.2-2 mM) onto the surface of the slice rapidly reduced or blocked the slow a.h.p. and the dendritic hyperpolarizing response to GABA. Intracellular injection of EGTA rapidly blocked the slow phase of the a.h.p. and then later blocked or reduced the dendritic hyperpolarizing response to GABA. We conclude that the hyperpolarizing response of the dendrites to GABA is mediated by a Ca2+-dependent K+ conductance.

Action Potentials↗
PubMed1982

gamma-Aminobutyric acid- and benzodiazepine-binding sites in human anterior pituitary tissue.

The existence of a gamma-aminobutyric acid (GABA) system in human anterior pituitary tissue was examined. Crude membrane fractions prepared from human anterior pituitary tissue bound tritiated GABA. The binding was saturable, and Scatchard analysis indicated a single binding site of high affinity (Kd = 40 nM) and a maximum binding of 1.2 pmol/mg protein. Binding was displaced in a dose-related manner by the GABA agonists muscimol (KI = 1 X 10(-8) M), isoguvacine (KI = 6 X 10(-7) M), THIP (4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridin-3-ol); KI = 5 X 10(-6) M), and the antagonist (+)bicuculline (KI = 5 X 10(-5) M) but not its inactive stereoisomer (-)bicuculline (KI greater than 10(-3) M). In anterior pituitary tissue, a significant concentration of GABA was found (mean, 2.5 +/- 0.5 nmol/mg protein) but no glutamic acid decarboxylase activity, the enzyme synthesizing GABA, was detected using a highly sensitive assay. In addition, benzodiazepine binding was present. An affinity of approximately 15 nM and a Bmax of approximately 0.75 pmol/mg protein were observed when using [3H]diazepam as the ligand. No saturable clonazepam binding occurred, and only slight GABA stimulation of diazepam binding was observed (mean, 18%; range, 6-38%). The ability of GABA and benzodiazepine to alter PRL secretion in rats suggests that the human pituitary GABA-binding sites described here might also mediate effects on PRL release.

Adult↗
PubMed1988

Carboxyethyl gamma-aminobutyric acid, a polyamine derivative, improves the recovery of EBV-transformed lymphocytes.

A polyamine derivative, carboxyethyl - Aminobutyric Acid (CEGABA), induces the formation of a large number of Epstein-Barr Virus (EBV) transformed lymphocytes, when added to the culture medium immediately after EBV infection. However, CEGABA shows only a moderate effect on the stability of EBV-transformed cell lines over time, and does not affect the growth of stabilized cell lines. It is possible that CEGABA acts on cells other than EBV transformed lymphocytes (in fact, after EBV infection all types of mononuclear cells from the blood are present in the culture) and indirectly promotes the growth of EBV transformed lymphocytes.

Antibodies, Monoclonal↗
PubMed1985

gamma-Aminobutyric acid enables synaptogenesis in the intact superior cervical ganglion of the adult rat.

Local gamma-aminobutyric acid (GABA) application into the intact superior cervical ganglion (SCG) of the adult rat allows active innervation of a surgically implanted hypoglossal nerve in addition to the normal nerve supply of the ganglion. In GABA-treated SCG of the adult rat, action potentials could be obtained on stimulation of both the preganglionic nerve trunk and the implanted hypoglossal nerve. Both action potentials were reversibly sensitive to hexamethonium bromide indicating new cholinergic synapses established between axons in the hypoglossal nerve and principal sympathetic neurons. If GABA treatment of the ganglion was omitted, the double innervation did not develop after hypoglossal nerve implantation.

Animals↗
PubMed2002

The neurotransmitter gamma-aminobutyric acid is an inhibitory regulator for the migration of SW 480 colon carcinoma cells.

Gamma-aminobutyric acid (GABA) is the inhibitory neurotransmitter in the brain, also playing a role in diseases like epilepsy. We now show that this inhibitory neurotransmitter can also reduce migratory activity in SW 480 colon carcinoma cells. GABA reduced the norepinephrine-induced migratory activity of these cells within a three-dimensional collagen matrix to spontaneous migration levels, as was analyzed by time-lapse videomicroscopy. This inhibitory effect of GABA was mediated by the serpentine receptor GABA(B) and was intracellularly transduced by a decrease of the cyclic AMP concentration. Cancer cell migration is thus regulated by neurobiological signals, opening new possibilities for pharmacological agonists in cancer therapy.

Bucladesine↗
PubMed1984

gamma-Aminobutyric acid activation of 36Cl- flux in rat hippocampal slices and its potentiation by barbiturates.

gamma-Aminobutyric acid (GABA) increases the rate of 36Cl- efflux from preloaded rat hippocampal slices in a dose-dependent manner (EC50: 400 microM). This action has the pharmacological specificity expected of activation of GABA receptors in that it is mimicked by the agonists muscimol and 3-aminopropanesulfonic acid, and blocked by the antagonists bicuculline and picrotoxinin. GABA uptake inhibitors, nipecotic acid and 2,4-diaminobutyric acid, fail to increase 36Cl- flux. Pentobarbital produces a dose-dependent activation (EC50 = 1.5 mM) of 36Cl- efflux with maximal response greater than that of GABA. The effect of pentobarbital can be mimicked by 1,3-dimethylbutylbarbiturate, secobarbital, (+)hexobarbital but not (-)hexobarbital, and is blocked by bicuculline and picrotoxinin. Pentobarbital and the other active barbiturates also potentiate the action of GABA. Phenobarbital does not have any effect independently or in combination with GABA. It is suggested that GABA increases 36Cl- permeability by activation of a postsynaptic receptor which is in turn functionally coupled to a barbiturate receptor.

Animals↗
PubMedDate not supplied

[Gamma-aminobutyric acid level and glutamate decarboxylase activity in the plasma of healthy persons].

Content of gamma-aminobutyric acid in blood plasma of healthy persons did not depend on sex and age and of women--on the phase of menstrual cycle. Activity of glutamate decarboxylase was higher 1.5-fold in blood plasma of women as compared with that of men values; a decrease in the enzymatic activity was observed in men after 30 years old and in women--after 40 years old. Activity of glutamate decarboxylase was higher in blood plasma of young and middle age women during the lutein phase of menstrual cycle as compared with the follicular phase, while this ratio reversed its direction in blood plasma of older women as a result of distinct decrease in the enzymatic activity during the lutein phase of the cycle.

Adolescent↗
PubMed1985

Autoreceptors regulate gamma-[3H]aminobutyric acid release from the guinea pig small intestine.

The possible presence of a presynaptic gamma-aminobutyric acid (GABA) receptor capable of regulating the release of GABA was investigated using the guinea pig small intestine. Muscimol at 10(-8) M and 10(-7) M, but not baclofen at 10(-6) M, inhibited the K+ (40 mM)-evoked Ca2+-dependent release of [3H]GABA from the small intestine preloaded with [3H]GABA, in the presence of 10(-6) M tetrodotoxin. The effect of muscimol on the K+-evoked GABA release was inhibited by bicuculline and furosemide. These results show that the guinea pig small intestine possesses presynaptic GABA receptors which may be involved in the regulation of the evoked GABA release. The presynaptic GABA receptor is bicuculline-sensitive and is probably coupled to the Cl- ion channel.

Animals↗
PubMed1987

Diazepam increases gamma-aminobutyric acid in human cerebrospinal fluid.

In 11 neurological patients, levels of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) were determined in cerebrospinal fluid (CSF) before and 1, 3, 5, and 8 min after intravenous injection of diazepam (2 or 5 mg). GABA levels increased progressively after intravenous injection of 5 but not 2 mg of the benzodiazepine, the differences from preinjection values being significant at 3, 5, and 8 min. Furthermore, when relative CSF GABA alterations determined after injection of diazepam were compared to those determined in sequential CSF aliquots of 10 patients without diazepam injection, mean GABA increases after diazepam were significantly different from controls in all CSF fractions. The data suggest that, in addition to its well-known effects on postsynaptic GABA function, diazepam may exert effects on endogenous GABA concentrations and/or on GABA release in the human CNS as reflected by elevation of GABA levels in human CSF.

Adult↗
PubMed1985

Serum gamma-aminobutyric acid (GABA) levels in patients with hepatic encephalopathy.

Serum levels of the potent inhibitory neurotransmitter gamma aminobutyric acid (GABA) were measured in 10 patients with chronic liver disease and hepatic encephalopathy, 11 patients with chronic liver disease and no evidence of hepatic encephalopathy, 7 patients with end-stage renal disease and 11 healthy volunteers. Serum GABA levels were elevated in all 10 patients with hepatic encephalopathy, 5/11 with liver disease and no encephalopathy and 4/7 renal disease patients. The mean serum GABA level for the encephalopathic patients (0.92 +/- 0.13 microM, mean +/- SEM) was significantly greater than the mean for liver disease patients without encephalopathy (0.48 +/- 0.05 microM, p less than 0.05), renal disease patients (0.46 +/- 0.04 microM, p less than 0.05) and healthy volunteers (0.39 +/- 0.03 microM, p less than 0.001). These results would tend to support the hypothesis that GABA may play a role in the pathogenesis of hepatic encephalopathy.

Ammonia↗
PubMed1980

A study of gamma-aminobutyric acid uptake in normal and Down's syndrome platelets.

1. Initial uptake rates of gamma-aminobutyric acid (GABA) were compared in Down's syndrome (D.S.) and normal platelets GABA uptake was decreased in D.S. platelets (1.10 +/- 0.10 nmol h-1 10(-9)) compared to uptake by normal platelets (1.89 +/- 0.21 nmol h-1 10(-9), P less than 0.005. 2. The effect of varying the NA+ concentration was similar on D.S. and normal platelets. Increasing the media Na+ concentration resulted in increased rates of GABA uptake in both D.S. and normal platelets. 3. GABA uptake in the presence of 2,4-dinitrophenol or at 2 degrees C is approximately 56% of the uptake at 37 degrees C for both D.S. and normal platelets. 4. Extrapolation of a reciprocal plot indicates a two affinity uptake system; a high affinity and a low affinity mechanism. 5. A significant defect in GABA uptake exists in D.S. platelets.

2,4-Dinitrophenol↗