Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMINOBUTYRIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,117 records · Page 62Linked to original sources
PubMed2002

Transport of 14C-gamma-aminobutyric acid into brain, cerebrospinal fluid and choroid plexus in neonatal and adult rats.

In general blood to brain entry of amino acids is greater in the neonatal rats compared to the adults. gamma-Aminobutyric acid (GABA), a neurotransmitter amino acid, shows limited transport across the blood-brain barrier (BBB) in the adult rat. Characteristics of GABA entry into the immature rat brain is yet to be addressed. This investigation was set to study the entry of GABA into brain of the neonatal rat compared to the adult. Using the bilateral in situ brain perfusion technique, the entry of 14C-GABA into brain, cerebrospinal fluid (CSF) and lateral ventricles choroid plexuses was studied in the adult and neonatal rats. 14C-GABA uptake into neonatal rat brain after 20 min perfusion was 0.116+/-0.014 ml g(-1), approximately twice that of the adults (P<0.01). Half saturation constant, K(m), did not change with age (P>0.05), whereas maximal transport into the brain, V(max), was reduced from 0.152 to 0.068 nmol min(-1) g(-1) showing a significant reduction with age (P<0.05). In the neonate the entry of GABA into the CSF was dominant when compared to that into the brain, this could be due to a greater diffusional component, K(d), which was detected to be high in the neonate. In conclusion, the uptake of 14C-GABA into brain of the immature rats exceeded that in the adults which is thought to be due to both greater maximal transport and greater diffusion in the neonate compared to the adult.

Aging↗
PubMed1984

Enhancement of high affinity gamma-aminobutyric acid receptor binding in cerebellum of pyridoxine-deficient rat.

The high-affinity of [3H]gamma-aminobutyric acid (GABA) to GABAA receptors and [3H]baclofen to GABAB receptors were studied in the cerebellum of pyridoxine-deficient rats and compared to pyridoxine-supplemented controls. There was a significant increase in the maximal binding (Bmax) of both GABAA and GABAB receptors with no significant difference in their binding affinities (Kd). The changes observed suggest a supersensitivity of GABAA and GABAB receptors which seems to correlate negatively with the concentration of GABA in the cerebellum of pyridoxine-deficient rats.

Animals↗
PubMed1992

Differing actions of beta-(2-thienyl)-gamma-aminobutyric acid in central and peripheral preparations.

In the guinea-pig isolated ileum, beta-(2-thienyl)-gamma-aminobutyric acid (BTG; 100-500 microM) reversibly and competitively (pA2 = 4.3 +/- 0.1) antagonised the baclofen-induced (5-100 microM) depression of cholinergic twitch contractions, but not that to adenosine or morphine. By contrast, in rat neocortical slice preparations, BTG (100-500 microM) acted as an agonist, abolishing the frequency and amplitude of spontaneous discharges, sensitive to 2-hydroxysaclofen (100-500 microM). BTG exhibits differential actions at GABAB receptors in brain and periphery.

Animals↗
PubMed1990

Comparison of transmitter amino acid levels in rat globus pallidus and neostriatum during hypoglycemia or after treatment with methionine sulfoximine or gamma-vinyl gamma-aminobutyric acid.

The levels of amino acids in globus pallidus, a structure heavily innervated with gamma-aminobutyric acid (GABA)-ergic terminals but few glutamergic terminals, were compared with the levels in neostriatum, a structure richly innervated with glutamergic terminals but intermediate in GABAergic terminals. The level of glutamate in neostriatum was twice as high as in globus pallidus whereas the level of GABA in globus pallidus was three times higher than in neostriatum. The level of aspartate was similar in both regions whereas the level of glutamine was correlated with the level of glutamate. Methionine sulfoximine, a glutamine synthetase inhibitor, reduced the level of glutamine to 10-20% of control in both structures. This reduction was accompanied by the largest decrease in the level of glutamate in neostriatum, indicating that transmitter glutamate turns over more rapidly than other glutamate pools. Likewise, insulin decreased the levels of glutamate and glutamine more in neostriatum than in globus pallidus. gamma-Vinyl GABA increased the level of GABA in globus pallidus more than in neostriatum although the percent increase was largest in neostriatum. Treatment with gamma-vinyl GABA was accompanied by a large reduction in the level of GABA, indicating that a substantial proportion of the glutamine pool is linked to GABA metabolism.

Amino Acids↗
PubMed1979

Central antihypertensive properties of muscimol and related gamma-aminobutyric acid agonists and the interaction of muscimol with baroreceptor reflexes.

The central antihypertensive properties of four gamma-aminobutyric acid (GABA) analogs were characterized in anesthetized cats with implanted intracerebroventricular cannulae. An intracerebroventricular infusion (icv) of muscimol, 0.1--0.5 microgram/min (total dose: 1--5 micrograms, icv), substantially reduced mean arterial pressure and slightly reduced heart rate. The compound was not hypotensive at 5 micrograms, iv (total dose) and only slightly hypotensive after an intracisternal injection (5 micrograms). Kojic amine (2-aminomethyl-5-hydroxy-4H-pyran-4-one) and baclofen were also hypotensive following an intracerebroventricular infusion, but they were less active than muscimol. GABA, at 15--150 micrograms/min, icv (total dose, 150--1500 micrograms, icv), was not hypotensive by itself and unlike muscimol its activity was not enhanced in cats pretreated with nipecotic acid, an uptake inhibitor of GABA. The ability of muscimol to interfere with baroreceptor reflexes was considered in experiments in which reflex vasoconstrictor (carotid occlusion) and reflex vasodilatation (acute elevation in mean arterial pressure with norepinephrine) was measured in the perfused hindlimb of cats previously prepared with intracerebroventricular cannulae. Muscimol significantly attenuated the response to bilateral carotid occlusion and completely abolished reflex vasodilatation. The results suggest that GABA agonists and analogs may regulate blood pressure centrally and, through an interaction with the central nervous system, may attenuate baroreceptor reflexes.

Animals↗
PubMed1983

Laminal distribution of gamma-aminobutyric acid (GABA) in the occipital cortex of rats: evidence as a neurotransmitter.

The laminal distribution of gamma-aminobutyric acid (GABA) in the rat occipital cortex was determined by an enzymatic procedure following decapitation or microwave irradiation (5 kW for 1.1 s). No significant differences were observed in the concentrations of GABA among 5 layers after microwave irradiation. However, when the animals were sacrificed by decapitation, the concentrations varied among the layers with the highest being detected in the internal granular layer (lamina IV) followed by the external granular (II), external pyramidal (III) and internal pyramidal layers (V). In these layers, GABA was significantly higher than in the other two layers, the molecular (I) and multiform layers (VI). The results are discussed in terms of the neurotransmitter function of GABA in the occipital cortex.

4-Aminobutyrate Transaminase↗
PubMed1978

The pharmacological properties of some crustacean neuronal acetylcholine, gamma-aminobutyric acid, and L-glutamate responses.

1. A study was performed of the L-glutamate, gamma-aminobutyric acid (GABA), and acetylcholine (ACh) responses of cells in the stomatogastric ganglion of the crab, Cancer pagurus. 2. Ionophoretic or pressure application of L-glutamate revealed three classes of responses: a K+-dependent inhibition which reversed at 15-20 mV more negative than the resting potential; a Cl- dependent inhibitory response which was at equilibrium at the resting potential; and a depolarizing response. 3. Ionophoretic or pressure applications of GABA likewise produced three kinds of responses: an increase in K+ conductance, an increase in Cl- conductance, and a depolarizing response. 4. Picrotoxin (10(-6)-10(-5) M) was effective in blocking both the glutamate inhibitory responses. 10(-4) M-picrotoxin, which was necessary to produce a 50% block of the GABA-K+-dependent response, had no effect on the GABA-Cl- response. 5. beta-Guanidinopropionic acid (beta-GP) was found to be an agonist for the GABA-K+ response, but was ineffective in mimicking or blocking the GABA-Cl- response. 6. ACh applications produced large depolarizing responses with a pharmacological profile similar to that of the nicotinic ganglionic response in vertebrates. 7. The muscarinic agonist, acetyl-beta-methyl choline (MeCh), produced depolarizations which decreased in amplitude as the membrane was hyperpolarized from -40 to -100 mV. Pilocarpine and oxotremorine produced changes in the endogenous activity of ganglionic neurones. 8. Implications of these results for the identification of synaptic transmitters in the somatogastric ganglion are discussed.

Acetylcholine↗
PubMed1986

Characterization of gamma-aminobutyric acid responses with sulfate loading in cat bladder neurons.

In some cells in cat bladder ganglia gamma-aminobutyric acid (GABA) applied iontophoretically produced a hyperpolarizing response accompanied by an increase in input conductance when recorded with potassium sulfate-filled microelectrodes. This GABA-induced hyperpolarization was blocked by bicuculline and was converted to a depolarizing GABA response when extracellular chloride concentration was low suggesting that the hyperpolarizing GABA response was mediated by the opening of chloride channels. In other cells, continuous passage of a small negative current converted a depolarizing GABA response to a hyperpolarizing response with time. This effect was accompanied by a negative shift of the reversal potential. These data indicated that injection of impermeable sulfate ions decreased the intracellular chloride concentration.

Adrenergic Fibers↗
PubMed1988

Fast HPLC estimation of gamma-aminobutyric acid in microdialysis perfusates: effect of nipecotic and 3-mercaptopropionic acids.

A method for rapid, automated (less than 5 min), and sensitive (detection limit 50 fmol/10 microliter) determination of gamma-aminobutyric acid (GABA) is described. The method is based on precolumn derivatization with o-phthaldialdehyde/t-butylthiol reagent and separation by reverse-phase HPLC with electrochemical detection under isocratic conditions. A 100 X 4 mm Nucleosil 3 C18 column was used; the mobile phase consisted of 0.15 M sodium acetate, 1 mM EDTA (pH 5.4), and 50% acetonitrile; the flow rate was 0.8 ml/min. The potential of the glassy carbon working electrode was +0.75 V. The method allows for the monitoring of GABA levels in the extracellular fluid sampled by microdialysis as documented in the present study when 0.5 mM nipecotic acid is infused via the probe, or 3-mercaptopropionic acid is injected at a dose of 100 mg/kg i.p. There was a 15-fold increase of extracellular GABA after nipecotic acid, whereas in the second case the inhibition of GABA synthesis was followed by a 74% decrease of GABA as compared to basal levels.

3-Mercaptopropionic Acid↗
PubMed1982

Central nervous system gamma-aminobutyric acid activity in man. Relationship to age and sex as reflected in CSF.

Central nervous system gamma-aminobutyric acid (GABA) activity was demonstrated to be an age- and sex-dependent phenomenon through the study of GABA concentration in lumbar CSF obtained from 87 drug-free normal individuals. Evaluation of the data from homogeneous subgroups of this population disclosed that both the propensity of lumbar CSF GABA levels to decrease with age and the magnitude of the rostrocaudal GABA concentration gradient are more pronounced in females, suggesting possible neuroendocrine involvement. Thus, age and sex are important variables that normally influence central GABAergic activity. Patient populations included in clinical investigations must be age- and sex-matched to avoid invalid conclusions biased by these physiologic variations in CSF GABA concentrations.

Adult↗
PubMed1982

The differential effect of ischemia on the active uptake of dopamine, gamma-aminobutyric acid, and glutamate by brain synaptosomes.

Ischemic stroke was induced in the Mongolian gerbil by left common carotid ligation. No change in uptake of [3H]dopamine, [3H]gamma-aminobutyric acid ([3H]GABA), or [14C]glutamate in synaptosomes obtained from the ischemic hemisphere was observed for up to 8 h. At 16 h after ligation, marked decrements in uptake were observed in animals showing hemiparesis: Uptake values expressed as a percent of the corresponding control hemisphere were 15.2% for dopamine, 28.9% for GABA, and 47.5% for glutamate. The differential sensitivity of dopamine terminals compared with glutamate terminals was highly significant. Separate experiments performed with synaptosomes isolated from the corpus striatum showed that the greater sensitivity to damage was intrinsic to the dopamine nerve terminal and not the result of regional variations in ischemic damage in brain. No bilateral effect of ischemia on dopamine uptake was evident. In animals exhibiting milder behavioral deficits (circling), a smaller and comparable decrement in uptake of dopamine, GABA, and glutamate was evident at 16 h, whereas animals not affected behaviorally showed no decrement at 16 h. Following uptake, the subsequent fractional release of neurotransmitter stimulated by 60 mM-potassium ions was not affected at any time point studied. Therefore, the loss in uptake at 16 h probably represents overt destruction of nerve terminals. Experiments with urethane used in place of pentobarbital for anesthesia during carotid occlusion showed that "protection" by pentobarbital was not a factor in the delayed response to ischemia. These results show that damage or destruction of nerve terminals is a delayed event following ischemia and that dopamine terminals are intrinsically more sensitive than glutamate terminals.

Animals↗
PubMed1995

[Effects of gamma-aminobutyric acid on isolated dog cerebral arteries].

The present experiments were designed to investigate the effects of gamma-aminobutyric acid (GABA) on isolated dog cerebral arteries (basilar artery). On addition of agonists phenylephrine 10 mumol.L-1, 5-HT 10 mumol.L-1, or KCl 25 mmol.L-1, the isometric tension of the contraction increased 0.51 +/- 0.18 g, 0.33 +/- 0.12 g and 0.57 +/- 0.16 g. After GABA at 50 mumol.L-1, the contraction was shown to decrease 0.27 +/- 0.15 g, 0.19 +/- 0.07 g and 0.17 +/- 0.06 g, the maximal relaxation were 45.49% +/- 20.4%, 58.60% +/- 12.96% and 27.75% +/- 15.78%, respectively. But it showed no effect on the contraction induced by high concentration of KCl (45 mmol.L-1). GABA also showed a potent relaxation on the contraction induced by cold Krebs solution (T 28 +/- 0.5 degrees C). The finding suggest that GABA can inhibit the muscle tone induced by various agonists and cooling in isolated dog basilar artery.

Animals↗
PubMed1996

gamma-Aminobutyric acid increases intracellular Ca2+ concentration in cultured cortical neurons: role of Cl- transport.

The effect of gamma-aminobutyric acid (GABA) on intracellular Ca2+ concentration ([Ca2+]i) in cultured prenatal rat cortical neurons was investigated using fluorescence imaging. GABA or muscimol, but not baclofen, increased [Ca2+]i in a dose-dependent manner. The GABAA receptor antagonists, bicuculline and picrotoxin, inhibited the GABA response. Furosemide, an inhibitor of the Na+/K+/2Cl- cotransporter, inhibited the GABA response in a noncompetitive manner. Ethacrynic acid, an inhibitor of an ATP-dependent Cl- pump, also inhibited the GABA-induced increased in [Ca2+]i. These results suggest a role for Cl- transport processes in the GABA response. The coapplication of GABA and high K+ led to a non-additive increase in the GABA response. The GABA response was also inhibited by nifedipine, a voltage-gated Ca2+ channel blocker, and abolished by the absence of extracellular Ca2+. Results indicate that the GABA response shares a common pathway of Ca2+ movement with the high K(+)-induced response. These observations suggest that the stimulation with GABA results in Ca2+ influx through voltage-gated Ca2+ channels, and that these effects are dependent on Cl- transport systems.

Animals↗
PubMed1981

The release of gamma-aminobutyric acid, glutamate, and acetylcholine from striatal slices: a mass fragmentographic study.

The release processes of endogenous Acetylcholine (ACh), gamma-aminobutyric acid (GABA), glutamate (Glu) and glutamine (GLN) were studied in superfused guinea-pig caudatal slices. Basal ACh release remained constant for up to 2 h, while the basal release of GABA, Glu and GLN declined to half or less of its initial values after 1 h of superfusion. Electrical stimulation increased the ACh release by 700-800% and that of GABA by 80% whereas it decreased the output of Glu by 50% and failed to modify the GLN efflux. KCl (25 nM) increased the output of ACh by 400%, that of GABA by approximately 500% and decreased that of Glu by 40%. Substituting of CaCl(2) by MgCl(2) in the superfusion medium reduced the basal efflux of GABA, Glu and GLN. Under these conditions, no evoked release of ACh or of GABA was detected, following electrical or KCl stimulation. Tetrodotoxin 5 x 10(-7) decreased the basal ACh release by 60% and increased the GABA efflux by 40%. The toxin abolished the stimulus-evoked ACh efflux but scarcely affected that of GABA. These results are consistent with a possible neurotransmitter role of ACh and GABA in the striatum and show some differences in the ionic mechanisms underlying GABA and ACh release.

Acetylcholine↗
PubMed1975

Binding of gamma-aminobutyric acid and taurine to synaptosomal fractions of regions of the feline CNS.

The "binding" of 3H-gamma-aminobutyric acid (3H-GABA) and 14C-taurine (7 X 10(-5) M) to synaptosomal fractions of the feline CNS was studied using differential centrifugation and double-isotope methods. Of the regions examined, the "binding" of GABA (in nmole/mg protein) occurred to the greatest extent, in cerebral cortex, olfactory bulb, and colliculi and, to a lesser extent, in caudate nucleus, corona radiata, and fornix. Distribution ratios revealed that GABA binding was greater in the cerebral cortex than in caudate nucleus, brain stem, spinal cord, and white matter regions. The binding of taurine (in nmole/mg protein) was lowest in cerebral cortex and highest in brain stem and spinal gray regions. Distribution ratios for taurine indicated that its accumulation was similar in all CNS regions studied, except for slightly higher values for cerebellar cortex and fornix. These results indicated that preferential binding of both GABA and taurine exists among regions of the feline CNS.

Aminobutyrates↗
PubMed1980

Effect of acute and repeated administration of gamma aminobutyric acid (GABA) on growth hormone and prolactin secretion in man.

A single oral dose of 5 g gamma aminobutyric acid (GABA) was given to 19 subjects and serial venous blood samples were obtained before and 3 h after drug administration. A placebo was administered to 18 subjects who served as controls. GABA caused a significant elevation of plasma growth hormone levels (P less than 0.001), but did not consistently alter plasma prolactin concentration since only 5 out of 15 subjects showed an increase of the hormone. Eight additional subjects were submitted to an insulin tolerance test before and after per os administration of 18 g GABA daily for 4 days. Protracted GABA treatment significantly blunted the response of growth hormone and enhanced that of prolactin to insulin hypoglycaemia (P less than 0.01). These results indicate that pharmacological doses of GABA affect growth hormone and prolactin secretion in man. The precise nature of GABA's effects as well as its mechanism of action remains to be clarified.

Administration, Oral↗
PubMed2006

Protective effect of gamma-aminobutyric acid (GABA) against cytotoxicity of ethanol in isolated rat hepatocytes involves modulations in cellular polyamine levels.

Gamma-aminobutyric acid (GABA) is considered to be a multifunctional molecule with various physiological effects throughout the body. It is also evident that the liver contains GABA and its transporter. However, the functions of GABA in liver have not been well documented. In this study, the cytoprotective effect of GABA against ethanol-induced hepatotoxicity was evaluated in primary cultured rat hepatocytes. Addition of ethanol induced decrease of cell viability in a dose-dependent manner. However, treatment with GABA resulted in a dose-dependent recovery from ethanol (150 mM)-induced cytotoxicity.GABA reversed the ethanol-induced decrease in intracellular polyamine levels. Furthermore, the addition of polyamines also reversed the ethanol-induced decrease of cell viability. These results suggest that GABA is protective against the cytotoxicity of ethanol in isolated rat hepatocytes and this effect may be modulated by the maintenance of intracellular polyamine levels.

Animals↗
PubMed2001

The pharmacology of gamma-aminobutyric acid and acetylcholine receptors at the echinoderm neuromuscular junction.

This review describes the various subtypes of gamma-aminobutyric acid (GABA) receptors found at the echinoderm neuromuscular junction (NMJ), based on pharmacological and physiological studies. The review focuses mainly on holothurian GABA receptors at the NMJ located between the radial nerve and longitudinal muscle of the body wall (LMBW) and compares them to GABA receptors described at other echinoderm NMJs. Since a primary action of GABA on the holothurian LMBW is to modulate contractile responses to the excitatory neurotransmitter, acetylcholine (ACh), the pharmacology of echinoderm nicotinic ACh receptors (nAChRs) and muscarinic ACh receptors (mAChRs) is also addressed. GABA responses have been described in the asteroids, echinoids and holothuroids but not in the other echinoderm classes. Some actions of GABA on echinoderm muscle include regulation of basal tone and spontaneous rhythmic contractions and modulation of cholinergic responses. Both GABA A and B receptor subtypes are present at the echinoderm NMJ, a feature also common to the arthropods, molluscs and chordates. Echinoderm GABA A receptors may mediate the excitatory responses to GABA. The GABA A receptor antagonist bicuculline has a paradoxical effect on contractility, stimulating large protracted contractions of the LMBW. The GABA A agonist muscimol potentiates cholinergic contractions of the holothurian LMBW. Another population of GABA receptors is inhibitory and is sensitive to the GABA B agonist baclofen and GABA B antagonists phaclofen and 2-OH-saclofen. The pre- and/or postsynaptic location of the GABA A and B receptors is not currently known. The folded GABA analogue 4-cis-aminocrotonic acid has no effect on the contractility of the holothurian LMBW so GABA C receptors are probably lacking in this preparation. Pharmacological studies have shown that distinct nAChRs and mAChRs are colocalized in numerous echinoderm muscle preparations. Most recently, nAChR agonists were used to characterize pharmacologically receptors at the holothurian LMBW that bind ACh. Nicotinic AChRs with unique pharmacological profiles are localized both pre- and postsynaptically at this NMJ, where their physiological action is to enhance muscle tone. Muscarinic agonists also have excitatory actions on the LMBW but their action is to stimulate phasic, rhythmic contractions of the muscle. The location of mAChRs at the echinoderm NMJ, however, is unknown. Since most of the studies described in the present review have used whole-mount preparations consisting largely of a combination of muscle fibers, neurons and connective tissue, it is extremely difficult to determine pharmacologically the exact location of the various receptor subtypes. Additional electrophysiological studies on isolated neurons and muscle fibers are therefore required to clearly define extra-, pre- and/or postsynaptic sites for the receptor subtypes at the echinoderm NMJ.

Acetylcholine↗