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 595 records · Page 33Linked to original sources
PubMed1982

Phosphatidylserine enhancement of [3H]gamma-aminobutyric acid uptake by rat whole brain synaptosomes.

[3H]gamma-Aminobutyric acid ([3H]GABA) binding to purified lipids was examined in an organic solvent-aqueous partition system. In addition, the [3H]GABA binding capacity in the partition system was compared with the capacity of lipids to alter sodium-dependent [3H]GABA uptake into synaptosomes isolated from rat whole brains. [3H]GABA was found to bind to all of the lipids studied in the organic solvent-aqueous partition system [phosphatidic acid (PA), phosphatidylethanolamine (PE), phosphatidylinositol (PI), phosphatidylserine (PS), gangliosides, and sulfatide], although PS exhibited the greatest binding capacity. [3H]GABA uptake into synaptosomes was enhanced by PS (48.0%) but was not altered by any other lipid. PS enhancement of [3H]GABA uptake required the presence of sodium and was blocked by nipecotic acid (10 microM). These results suggest that PS may play a role in the sodium-dependent GABA reuptake process in the presynaptic nerve end.

Animals↗
PubMed2004

The interaction between gamma-aminobutyric acid agonists and diltiazem in visceral antinociception in rats.

UNLABELLED: To examine whether the gamma-aminobutyric acid (GABA) receptor agonists and L-type voltage-dependent calcium channel blockers potentiate each other on the visceral antinociceptive effects at the spinal cord, we assessed visceral nociception with colorectal distension (CD) test in rats with an intrathecal catheter. The measurements were performed after intrathecal administration of a GABA agonist (muscimol or baclofen), a calcium channel blocker (diltiazem), or the combination of the two. CD threshold did not change after muscimol 0.1 microg, baclofen 0.01 microg, or diltiazem 100 microg, but increased slightly after muscimol 1 microg and baclofen 0.1 microg. When muscimol 0.1 microg or 1 microg was administered with diltiazem, the increase in CD threshold was significantly larger than muscimol alone (at 5 min, 26.2% versus 0.6% MPE (maximum possible effect) or 84.5% versus 19.5%MPE, respectively; P < 0.01). The CD threshold after the combination of baclofen 0.1 microg and diltiazem also showed a significantly larger increase than that seen after baclofen alone (at 5 min, 48.0% versus 14.3% MPE; P < 0.01). Motor paralysis observed with muscimol 1 microg did not increase when muscimol was coadministered with diltiazem. In conclusion, intrathecal diltiazem in combination with a GABA agonist, muscimol or baclofen, potentiated the GABA agonists-induced visceral antinociception without increasing motor paralysis. IMPLICATIONS: Intrathecal administration of diltiazem in combination with a gamma-aminobutyric acid (GABA) agonist, muscimol or baclofen, potentiated the GABA agonists-induced visceral antinociception but did not affect motor paralysis. The present results indicate that the coadministration of the two types of drugs may be clinically useful.

Animals↗
PubMed1982

Inhibitory effects of motilin, somatostatin, [Leu]enkephalin, [Met]enkephalin, and taurine on neurons of the lateral vestibular nucleus: interactions with gamma-aminobutyric acid.

Motilin, [Met]enkephalin, [Leu]enkephalin, somatostatin, taurine, gamma-aminobutyric acid (GABA), and glycine were tested for their effects on Deiters neurons of the lateral vestibular nucleus in rabbits. Iontophoresis was carried out with multibarrelled micropipettes. All four peptides and three amino acids produced depression of neuron firing. No facilitatory responses were observed. The depressant action of each peptide when iontophoresed alone was dose-dependent and was rapid in onset and recovery. Their characteristic actions suggest the possibility of their independent roles as strong inhibitors, although the experimental paradigm does not allow conclusions about the individual potency of each peptide. When GABA was administered together with motilin, [Met]enkephalin, or somatostatin, the effects of the peptide and GABA were additive, producing depression greater than that with application of either substance alone. When GABA was applied in conjunction with [Leu]enkephalin, more complex interactions were observed. At low iontophoretic currents, [Leu]enkephalin antagonized the action of GABA, producing a depression less than that of GABA alone and of considerably slower onset, suggesting an additional modulatory effect. These observations support the conclusion that all substances tested are chemical mediators in the lateral vestibular nucleus and [Leu]enkephalin may be a neuromodulator as well. Because recent immunocytochemical studies indicate that Purkinje cells in the cerebellar cortex are chemically heterogeneous and exhibit immunoreactivity for motilin, taurine, the enkephalins, and somatostatin, as well as for the GABA-synthesizing enzyme glutamic acid decarboxylase, it is suggested that the Purkinje cell projections to vestibular and cerebellar nuclei are multimodal in their chemical coding. The uniformly depressant action of the peptides and amino acids reported here is consistent with earlier observations that Purkinje cells exert an inhibitory influence on the vestibular and central cerebellar nuclei.

Action Potentials↗
PubMed1980

Interplexiform cell in cat retina: identification by uptake of gamma-[3H]aminobutyric acid and serial reconstruction.

After intravitreal injection of gamma-[3H] aminobutyric acid (GAB), 2% of the neurons at the outer margin of the inner plexiform layer were intensely labeled. Reconstructions of these neurons from serial electron microscope autoradiograms showed that they are interplexiform cells, which synapse on bipolar processes in the outer plexiform layer and on amacrine and bipolar processes in the inner plexiform layer.

Animals↗
PubMedDate not supplied

Influence of new gamma-aminobutyric acid amide derivatives and its phthalimide precursors on the central nervous system activity in mice.

The present study investigated the influence of BM-78, BM-121 (gamma-aminobutyric acid amide derivatives) and BM-42, BM-43 (phthalimide precursors of BM-78 and BM-121) on the spontaneous locomotor activity and on the picrotoxin-induced seizures. Results of pharmacological in vivo examination of the effects of new gamma-aminobutyric acid amide derivatives and its phthalimide precursors (compounds BM-78, BM-121, BM-42, BM-43), presented in this paper showed that all the compounds had different but clear influence on CNS in mice.

Animals↗
PubMed1982

Effect of calcium ion on the release of gamma-aminobutyric acid from synaptosomal fraction.

Brain synaptosomes released endogenous gamma-aminobutyric acid (GABA) in response to Ca2+. The release of GABA in response to 2.5 mM Ca2+ increased linearly with log[K+]0, showing that a membrane potential-dependent Ca2+ channel limits the GABA release. In the presence of Ca2+ ionophore, A23187, GABA release increased linearly with log[Ca2+]0 without altering the membrane potential of synaptosomes.

Animals↗
PubMed1986

Low levels of gamma-aminobutyric acid in cerebrospinal fluid of dogs with epilepsy.

gamma-Aminobutyric acid (GABA) levels were determined in cisternal cerebrospinal fluid (CSF) of 19 epileptic dogs with generalized tonic-clonic (grand mal) seizures using a radioreceptor assay. Thirty-four healthy age-matched dogs served as controls. The average CSF GABA level in epileptic dogs (40 pmol/ml) was significantly lower than that determined in controls (66 pmol/ml). Treatment with phenobarbital or primidone seemed not to affect CSF GABA levels.

Animals↗
PubMed1980

New anticonvulsants: Schiff bases of gamma-aminobutyric acid and gamma-aminobutyramide.

Schiff bases of gamma-aminobutyric acid (gammaAbu) and gamma-aminobutyramide (gammaAbuNH2) were prepared and tested for anticonvulsant and gammaAbu mimetic activity. 4-[[(4-Chlorophenyl)(5-fluoro-2-hydroxyphenyl)methylene]amino]butanoic acid monosodium salt (4) and 4-[[(4-chlorophenyl)(5-fluoro-2-hydroxyphenyl)methylene]amino]butanamide (5) blocked bicuculline-induced lethality and convulsions and displaced [3H]gammaAbu from its membrane binding sites. In the rat dorsal root sensory ganglion, compound 4 exhibited gammaAbu agonist properties. Compounds 4 and 5 are thus anticonvulsants and directly acting gammaAbu mimetics.

Animals↗
PubMed2001

Anti-ischemic and cognition-enhancing properties of NNC-711, a gamma-aminobutyric acid reuptake inhibitor.

NNC-711 [1-(2-((diphenylmethylene)amino)oxy)ethyl)-1,2,4,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride], a gamma-aminobutyric acid (GABA) reuptake inhibitor with anticonvulsant activity, was investigated with respect to its cognition-enhancing and neuroprotective potency. In the rat, administration of NNC-711 immediately prior to training prevented amnesia for a passive avoidance task induced by the acetylcholine receptor antagonist scopolamine. NNC-711 was also effective in protecting against ischemia-induced death of CA1 pyramidal neurons in a model of bilateral common carotid artery occlusion in the gerbil. In addition to a neuroprotective activity, NNC-711 exhibited significant cognition-enhancing actions. Daily administration of NNC-711, immediately prior to a spatial learning task, significantly reduced escape latencies in the water maze paradigm in both mature (postnatal day 80) and aged (28 months) rats. All of the above actions exhibited a bell-shaped response with an optimal dose of 0.5-1.0 mg/kg. These investigations with NNC-711 and previous clinical observations on the structurally related anticonvulsant tiagabine confirm the potential of GABA reuptake inhibitors as anti-amnesia and cognition-enhancing agents.

Amnesia↗
PubMed2004

Statistical mechanics model for the interaction between the neurotransmitter gamma-aminobutyric acid and GABAA receptors.

Interactions between the neurotransmitter gamma-aminobutyric acid (GABA) and GABAA receptor ion channels play an important role in the central nervous system. A statistical mechanics model is proposed for the interaction between GABA and GABAA receptors. The model provides good fits to the electrophysiology data as well as an estimation of receptor activation energies, and predicts the temperature dependence consistent with measurements. In addition, the model provides insights into single channel conductance measurements. This model is also applicable to other ligand-gated ion channels with similar pentameric structures.

Biophysical Phenomena↗
PubMed1985

Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder.

The presence of gamma-aminobutyric acid (GABA)-ergic neuron in guinea pig gallbladder was investigated by measuring GABA contents and glutamate decarboxylase (GAD) activity and by demonstrating the uptake and release of [3H]GABA. GABA and GAD are both present in the gallbladder, and a positive correlation in regional distribution was observed among GABA, GAD, and the number of ganglion cells. The uptake of [3H]GABA by the gallbladder showed two saturable components; a high-affinity component (Km = 23.3 microM, Vmax = 7.63 nmol X g-1 X 10 min-1) and a low-affinity component (Km = 515 microM, Vmax = 57.1 nmol X g-1 X 10 min-1). These high-affinity and low-affinity transport systems corresponded to those obtained in the presence of beta-alanine and L-2,4-diaminobutyric acid, respectively, thereby suggesting the presence of neuronal and nonneuronal GABA transport systems in this tissue. Electrical transmural stimulation produced an increase in [3H]-GABA release from the isolated gallbladder preloaded with [3H]GABA, in the presence of beta-alanine. The stimulation-evoked release of [3H]GABA was prevented by calcium-free medium containing 1 mM EGTA and tetrodotoxin, thereby indicating that the released GABA originates from the nerve terminals. These results provide evidence for the presence of GABA-ergic neurons in the guinea pig gallbladder.

Animals↗
PubMed1986

Gamma-aminobutyric acid (GABA) production by eight common bacterial pathogens.

Gamma-aminobutyric acid (GABA) is a potent amino acid neurotransmitter that suppresses normal neuronal activity in the central nervous system. Recently it has been suggested that GABA may play an important role in the pathogenesis of hepatic encephalopathy. In the present study GABA production by 8 common bacterial pathogens was measured during mid-log, stationary and mid-death phases of growth. All bacteria produced some GABA (range: 160-50 250 pmole/ml) with the majority of GABA production occurring during the mid-death phase of growth. These results suggest that the depressed levels of consciousness seen in patients with overwhelming sepsis or advanced liver disease and extraintestinal infection may in part be secondary to increased bacterial GABA production.

Bacteria↗
PubMed1987

Chloride channels activated by gamma-aminobutyric acid in normal bovine lactotrophs.

The effect of gamma-aminobutyric acid (GABA) on normal bovine lactotrophs was investigated using the patch clamp technique. GABA application (1-10 microM) induced fluctuations of membrane current, accompanied by an increase in inward current. The mean conductance of GABA-activated channels was estimated to be 19 pS from statistical analysis of these fluctuations whereas the mean conductance for GABA-activated single ion channels was 16 pS. The reversal potential of the current was near to the equilibrium potential for chloride ions. These results indicate that the one possible mechanism for inhibition of prolactin release induced by GABA is probably mediated by activation of chloride channels.

Animals↗
PubMed2005

Alleviative effects of gamma-aminobutyric acid (GABA) on behavioral abnormalities in aged dogs.

gamma-aminobutyric acid (GABA, 30 mg/kg) was administered to aged dogs with recent history of veterinary clinic visits (mean age: 15.3 years old) once daily for 2 weeks by mixing with food. Their owners subjectively evaluated the effects of GABA on behavioral signs often associated with aging in the dogs. Improvement in some of behavioral signs was notable without any observable adverse effects. Dogs administered with GABA tended to exhibit improvement in emotional states and signs may be caused by neurovegetable dysfunction, though effects on cognitive dysfunction syndrome were not always observed. Thus, GABA administration may be one of the effective means of improving the quality of life of aged dogs.

Aging↗
PubMed1984

Gamma-aminobutyric acid and basal ganglia outflow pathways.

Neurons containing gamma-aminobutyric acid (GABA) are important outflow pathways from the striatum to the pallidal complex and substantia nigra. From these areas GABA-containing neurons pass to the thalamus and to various areas of the brainstem. Manipulation of GABA function in outflow zones in the rat can produce catalepsy, locomotor hyperactivity, stereotypy or circling behaviour, so mimicking the effect of altered dopamine function within basal ganglia. However, the behaviours produced by such manipulation do not form part of the animal's normal activities. Consequently manipulation of GABA action in the outflow zones of the basal ganglia may mimic extrapyramidal movement disorders more closely than the normal functions of these regions of the brain.

Animals↗
PubMed1993

Isocratic HPLC assay with electrochemical detection of free gamma-aminobutyric acid in cerebrospinal fluid.

A method for measuring gamma-aminobutyric acid (GABA) in human cerebrospinal fluid (CSF) by isocratic HPLC with electrochemical detection is described. The method is based on precolumn derivatization of GABA with o-phthaldialdehyde (OPA) and tert-butylthiol (t-BT), separation of the GABA-OPA complex on a reversed-phase column, and quantitation by means of a Coulochem electrochemical detector. The method is highly sensitive and specific for GABA. In three samples of human CSF containing low, medium, and high amounts of GABA, the coefficients of variation between and within runs were 4.5% and 3.6%, respectively. The concentration of GABA in 10 neurologically intact subjects was 92.5 +/- 9.4 nmol/L of CSF.

Adolescent↗
PubMed1984

Diazotization and thiocyanate differentiate agonists from antagonists for the high- and low-affinity receptors of gamma-aminobutyric acid.

The differentiation of high- and low-affinity postsynaptic gamma-aminobutyric acid (GABA) receptors was examined in a washed cortical membrane preparation of the rat. The selective elimination of the high- and low-affinity GABA sites by the chaotropic anion thiocyanate and diazotization by p-diazobenzenesulfonic acid (DSA), respectively, offered two model systems for the separate sites. The [3H]GABA displacing potencies of some GABA agonists [GABA, 4,5,6,7-tetrahydro- isoxazole [4,5c]pyridine-3-ol (THIP), and muscimol] and antagonists [bicuculline methiodide (BCM), 3-alpha-hydroxy-16-imino-5 beta-17-aza-androstan-11-one (R-5135), and d-tubocurarine] and their slope factors were examined in these model systems and in control membranes. The displacing potency of the agonists was increased in the DSA-pretreated membranes and decreased in the presence of thiocyanate. The displacing potency of the antagonists was shifted in an opposite manner. The chaotropic effect of thiocyanate was reversible and not additive with the inhibitory effect of diazotization on the specific binding of GABA. Inhibition of specific GABA binding by pyridoxal-5-phosphate (PLP) could not be protected by GABA antagonists (BCM and R-5135) but only by agonists. The results can be interpreted in the framework of a dual (agonist-antagonist) receptor model, postulating a hydrophobic accessory site at the low-affinity GABA receptor. The effect of thiocyanate on the GABA receptor may result in the exposure of the hydrophobic accessory sites.

Androstanes↗