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At least 199 records · Page 11Linked to original sources
PubMed1980

(+/-)-trans-2-(Aminomethyl)cyclobutanecarboxylic acid hydrochloride: a rigid analogue of gamma-aminobutyric acid.

The (+/-) title compound was prepared to evaluate prior observations that certain gamma-aminobutyric acid (gamma Abu) congeners in the transoid disposition demonstrate gamma Abu receptor binding activity. It was prepared by a multistep sequence from (+/-)-methyl trans-2-(hydroxymethyl)cyclobutanecarboxylate. In a sodium-independent binding assay, the specific binding of (+/-)-1 to synaptic membranes from rat brain tissue was 1/14 500 that of gamma Abu.

Animals↗
PubMed1998

Production of gamma-aminobutyric acid by cheese starters during cheese ripening.

Nine mixed-strain starters were examined for their abilities to produce gamma-aminobutyric acid. Six commercial starters were found to produce gamma-aminobutyric acid in a skim milk culture. The bacterium that produced gamma-aminobutyric acid was isolated from the mixed-strain starters, identified as citrate-utilizing Lactococcus lactis ssp. lactis (formerly L. lactis ssp. lactis biovar diacetylactis) and designated as strain 01-7. A cell extract showed glutamate decarboxylase activity, for which the optimum pH was 4.7. In pH-controlled cultivation, gamma-aminobutyric acid was generated at pH 5.0 but not above pH 5.5. Cheeses were prepared experimentally using strain 01-7 to determine the relationship between the pH values and the production of gamma-aminobutyric acid during cheese ripening. gamma-Aminobutyric acid increased linearly in the experimental cheeses as the pH of the cheese decreased. Based on these results, gamma-aminobutyric acid was concluded to be produced by the cheese starters during ripening.

Cheese↗
PubMed1981

Inhibition of vasopressin release to carotid occlusion by gamma-aminobutyric acid and glycine.

1 In cats anaesthetized with pentobarbitone sodium or chloralose, the amino acids, gamma-aminobutyric acid (GABA) and glycine, were applied to the ventral surface of the brain through paired Perspex rings placed across the medulla. 2 Applied to a region situated at the transition between medulla and cord, both amino acids greatly attenuated and even abolished the vasopressin release in response to carotid occlusion. Glycine was about 100 times more potent than GABA and effective in a concentration of 0.1 mg/ml. The pressor response to carotid occlusion was not affected. 3 Applied to a region situated 5 to 6 mm more rostrally, the amino acids did not affect vasopressin release but in strong concentrations, greatly attenuated the pressor response to carotid occlusion. 4 The two responses to carotid occlusion, vasopressin release and the pressor response, can thus be influenced independently. 5 It is concluded that the pathways carrying afferent impulses from the baroreceptors in the carotid sinus reach the ventral surface of the brain stem at two regions. At both, synaptic transmission can be blocked by the application of an inhibitory amino acid and thus prevent either the release of vasopressin at the caudal site, or the increase of vasomotor tone at the rostral site.

Animals↗
PubMed1990

[3H]nipecotic acid binding to gamma-aminobutyric acid uptake sites in postmortem human brain.

Binding of [3H]nipecotic acid, a proposed marker for GABAergic neurons, was investigated in postmortem human brain by use of a centrifugation assay. Binding was displaceable, apparently saturable, and to a single site, with typical KD and Bmax values of 1.85 microM and 124.2 pmol/mg of protein in the hippocampus. Regional distribution studies indicated a heterogeneous population of [3H]nipecotic acid binding sites with highest concentrations in the lateral globus pallidus. Putamen tissue from four cases of Huntington's disease showed a marked reduction in [3H]nipecotic acid binding. Binding correlated with both age and postmortem delay in the hippocampus. There was an effect of agonal state in which prolonged illness before death apparently caused a reduction in binding. Our results indicate that [3H]nipecotic acid may be used successfully as a marker for neuronal GABAergic uptake sites in human brain, but that the effects of variables such as age, postmortem delay, and agonal state must always be taken into account.

Aged↗
PubMed1994

gamma-Aminobutyric acid in the nervous system of a planarian.

The amino acid gamma-aminobutyric acid (GABA) is an important inhibitory neurotransmitter in both vertebrates and invertebrates. Despite this, no reports of GABA in flatworms have to date been published. We have studied the presence of GABA in the planarian Dugesia tigrina with immunocytochemical methods and high-pressure liquid chromatography. Fibers showing GABA-like immunoreactivity (GABA-IR) were present in abundance in the longitudinal nerve cords and lateral nerves. GABA-IR was revealed in fibers forming commissures in the brain. The ventral part of the subepidermal plexus showed GABA-IR. No cell somata containing GABA-IR could be identified with certainty. The chromatographic analysis showed that the average GABA concentration in D. tigrina is 533.6 pmol/mg protein. This is substantially higher than the concentrations of dopamine (62.87 pmol/mg) and serotonin (233.20 pmol/mg). An enzyme assay confirmed the capacity for GABA-synthesis in D. tigrina. The results indicate that GABA-containing neurons appeared earlier in evolution than was previously thought and that GABA may serve an important role already in the flatworms.

Animals↗
PubMed1996

gamma-Aminobutyric acid and glycine in the baboon cochlear nuclei: an immunocytochemical colocalization study with reference to interspecies differences in inhibitory systems.

Previous studies of the cochlear nuclei in cat, rat, and guinea pig have demonstrated neural structures that are enriched in the inhibitory neurotransmitter amino acids gamma-aminobutyric acid (GABA) and glycine. In these mammals, inhibitory terminals are widely distributed throughout the nuclear complex, but somata of inhibitory neurons are concentrated in the dorsal cochlear nucleus, in granule cell regions, and in the cap area. Because these are the subdivisions that undergo the most pronounced phylogenetic changes in primates, we wanted to see whether the inhibitory systems are influenced by changes in cytoarchitecture. Therefore, we applied light microscopic postembedding immunostaining and optical densitometry to the cochlear nuclei of an anthropoid primate, the Senegalese baboon (Papio anubis). Our results demonstrate that, in baboon 1) glycinergic neurons and axons in the ventral cochlear nucleus seem to form a commissural system similar to that of other mammals; 2) the tuberculoventral system appears to be unchanged in morphology but exhibits a higher level of colocalization of GABA with glycine; 3) there is a reduction of the granule/cartwheel cell system, which is reflected in lesser numbers of inhibitory cartwheel, Golgi, and molecular layer stellate cells; 4) the cap area is larger than in rodents and carnivores and contains many neurons that colocalize GABA and glycine; and 5) throughout the nuclear complex, a higher proportion of the inhibitory terminals colocalize GABA and glycine. We conclude that modulation of the ascending auditory pathway in baboon is likely to differ from that in rodents and cat.

Animals↗
PubMed1999

theta, a novel gamma-aminobutyric acid type A receptor subunit.

gamma-Aminobutyric acid type A (GABA-A) receptors are a major mediator of inhibitory neurotransmission in the mammalian central nervous system, and the site of action of a number of clinically important drugs. These receptors exist as a family of subtypes with distinct temporal and spatial patterns of expression and distinct properties that presumably underlie a precise role for each subtype. The newest member of this gene family is the theta subunit. The deduced polypeptide sequence is 627 amino acids long and has highest sequence identity (50.5%) with the beta1 subunit. Within the rat striatum, this subunit coassembles with alpha2, beta1, and gamma1, suggesting that gamma-aminobutyric acid type A receptors consisting of arrangements other than alpha beta + gamma, delta, or epsilon do exist. Expression of alpha2beta1gamma1theta in transfected mammalian cells leads to the formation of receptors with a 4-fold decrease in the affinity for gamma-aminobutyric acid compared with alpha2beta1gamma1. This subunit has a unique distribution, with studies so far suggesting significant expression within monoaminergic neurons of both human and monkey brain.

Amino Acid Sequence↗
PubMed1985

Synthesis of acetylcholine and gamma-aminobutyric acid by dissociated cerebral cortical cells in vitro.

Biosynthesis of acetylcholine and gamma-aminobutyric acid was investigated in primary cultures derived from embryonic rat cerebral cortex. The cortical cultures contained a mixture of neurons and non-neuronal cells. Cortical neurons were viable for at least 2 months in vitro. The cultures accumulated [3H]choline from the medium and synthesized acetylcholine. Choline uptake was significantly reduced by hemicholinium-3 and acetylcholine synthesis by intact cultures was partially inhibited by naphthylvinylpyridine. In lysed cultures, greater than 90% of acetylcholine synthesizing activity was inhibited by naphthylvinylpyridine. Acetylcholine synthesis and storage by intact cells increased as the concentration of choline increased and approached saturation near 50 microM choline. Also, the synthesis and storage of gamma-aminobutyric acid from [3H]glutamate increased as the concentration of glutamic acid increased and began to saturate near 25 microM glutamate. The rates of synthesis of acetylcholine from 5 microM choline and of gamma-aminobutyric acid from 50 microM glutamate were linear for at least 30 min. The synthesis and accumulation of acetylcholine and gamma-aminobutyric acid from their respective precursors showed a similar dependence on culture age; they increased constantly during the first 3 weeks in culture, thereafter they declined. Mixed cultures of cortical cells and either skeletal muscle or various other non-neuronal cells exhibited a 40-100% enhancement in both acetylcholine and gamma-aminobutyric acid synthesis. Autoradiographic methods showed that a subpopulation of neurons in the cortical cultures accumulated gamma-aminobutyric acid from the medium.

Acetylcholine↗
PubMed1982

gamma-Aminobutyric acid and benzodiazepine binding sites in audiogenic seizure-susceptible mice.

The properties of gamma-aminobutyric acid recognition sites, benzodiazepine binding sites and the effect of exogeneous gamma-aminobutyric acid on benzodiazepine binding were determined in crude membrane fractions prepared from the brains of DBA/2 mice at ages before (8-9 and 17-18 days), during (22-23 and 28-29 days) and after (40-43 days) the age of high susceptibility to audiogenic seizures. These have been compared with data from age-matched mice of a strain (TO) with lower audiogenic seizure susceptibility. The number of high-affinity [3H]gamma-aminobutyric acid binding sites was lower at all ages in DBA/2 mice compared with TO mice, but the affinity was higher in DBA/2 mice. The number of low-affinity [3H]gamma-aminobutyric acid binding sites was lower at 8-9 days and 40-43 days in DBA/2 mice, but was not significantly different from TO mice at other ages. For [3H]flunitrazepam binding, the only difference found was a slight reduction in the number of binding sites at 28-29 days of age in DBA/2 mice. gamma-Aminobutyric acid stimulation of [3H]flunitrazepam binding was not significantly different up to 22-23 days of age, but was higher in DBA/2 mice at 28-29 days and lower at 40-43 days. Impairment of gamma-aminobutyric acid function is a possible permissive factor in the age-dependent audiogenic seizure susceptibility in DBA/2 mice.

Acoustic Stimulation↗
PubMed1996

Evidence for release of glutamic acid, aspartic acid and substance P but not gamma-aminobutyric acid from primary afferent fibres in rat spinal cord.

In vitro superfusion release experiments and autoradiography were carried out on spinal cords of neonatally capsaicin-treated rats. Electrical and chemical stimulations significantly increased the release of aspartate, glutamate and gamma-aminobutyric acid (GABA) from hemisected dorsal horn slices of vehicle-treated animals. In capsaicin-treated rats, the evoked release of aspartate, glutamate and substance P but not GABA, were significantly lower. Capsaicin (1 microM) stimulated the release of aspartate and glutamate, as reported for substance P, in control slices but this effect was not as apparent in tissues from capsaicin-treated rats. Evoked GABA release was not affected in either case. alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, dizocilpine and GABAB binding sites were highly localised in the substantia gelatinosa. Capsaicin treatment did not affect the affinity of the binding sites in all four cases but significantly reduced the density of kainate, dizocilpine and GABAB binding sites. The data suggest that capsaicin-sensitive primary afferent fibres release aspartate, glutamate and Substance P following high-intensity stimulations and that this release might be modulated by presynaptic glutamate and GABAB receptors present on these terminals.

Afferent Pathways↗
PubMed1984

Different types of potassium transport linked to carbachol and gamma-aminobutyric acid actions in rat sympathetic neurons.

Carbachol and gamma-aminobutyric acid depolarize mammalian sympathetic neurons and increase the free extracellular K+-concentration. We have used double-barrelled ion-sensitive microelectrodes to determine changes of the membrane potential and of the free intracellular Na+-, K+- and Cl- -concentrations ( [Na+]i, [K+]i and [Cl-]i) during neurotransmitter application. Experiments were performed on isolated, desheathed superior cervical ganglia of the rat, maintained in Krebs solution at 30 degrees C. Application of carbachol resulted in a membrane depolarization accompanied by an increase of [Na+]i, a decrease of [K+]i and no change in [Cl-]i. Application of gamma-aminobutyric acid also induced a membrane depolarization which, however, was accompanied by a decrease of [K+]i and [Cl-]i, whereas [Na+]i remained constant. Blockade of the Na+/K+-pump by ouabain completely inhibited both the reuptake of K+ and the extrusion of Na+ after the action of carbachol, and also the post-carbachol undershoot of the free extracellular K+-concentration. On the other hand, in the presence of ouabain, no changes in the kinetics of the reuptake of K+ released during the action of gamma-aminobutyric acid could be observed. Furosemide, a blocker of K+/Cl- -cotransport, inhibited the reuptake of Cl- and K+ after the action of gamma-aminobutyric acid. In summary, the data reveal that rat sympathetic neurons possess, in addition to the Na+/K+-pump, another transport system to regulate free intracellular K+-concentration. This system is possibly a K+/Cl- -cotransport.

Animals↗