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PubMed1982

A presumptive role for gamma-aminobutyric acid in the regulation of gonadotropin secretion in man.

The effect of di-n-propylacetic acid (valproic acid), a gamma-aminobutyric acid transaminase inhibitor, on the luteinizing hormone (LH) and follicle-stimulating hormone (FSH) response to gonadotropin-releasing hormone (LHRH) was studied in five normal women during the proliferative and luteal phases of the menstrual cycle. Valproic acid produced no significant change in the basal serum concentrations of LH, FSH, estradiol, and progesterone in either the proliferative or the luteal phase of the study. In the proliferative phase the delta LH (maximum increment above baseline) following LHRH stimulation rose from 32.8 +/- 21.2 (mean +/- SD) to 52.2 +/- 28.7 mlU/ml (not significant) after valproic acid, while the delta FSH rose from 2.2 +/- 1.1 to 5.0 +/- 3.6 mlU/ml (not significant). Four of the five volunteers showed an augmentation of the delta LH response to LHRH after valproic acid while the fifth subject showed no change. In three subjects the augmented delta LH response after valproic acid was highly significant. By contrast, the delta LH in the luteal phase following LHRH stimulation fell from 65.3 +/- 20.1 to 43.1 +/- 12.9 mlU/ml after valproic acid (p less than 0.03). Corresponding delta FSH values were 2.5 +/- 1.1 and 2.1 +/- 0.8 mlU/ml (not significant). It is speculated that gamma-aminobutyric acid may exert a modulatory role on gonadotropin secretion following LHRH stimulation and that this effect is influenced by the phase of the menstrual cycle.

Adult↗
PubMed2006

Regulation of Arabidopsis thaliana 14-3-3 gene expression by gamma-aminobutyric acid.

The function in plants of the non-protein amino acid, gamma-aminobutyric acid (GABA) is poorly understood. In this study, we show that GABA down-regulates the expression of a large subset of 14-3-3 gene family members in Arabidopsis thaliana seedlings in a calcium, ethylene and abscisic acid (ABA)-dependent manner. Gene expression is not affected when seedlings are supplied with glutamate (GLU), a precursor of GABA. The repression of 14-3-3 gene expression by GABA is dependent on functional ethylene and ABA signalling pathways, because the response is lost in the etr1-1, abi1-1 and abi2-1 mutants. Calcium measurements show that in contrast to GLU, GABA does not elicit a cytoplasmic calcium elevation, suggesting that the GABA response is unlikely to be mediated by GLU receptors (GLRs), as has been suggested previously. We suggest that in addition to its role as a stress-related metabolite, GABA may regulate gene expression in A. thaliana, including members of the 14-3-3 gene family.

14-3-3 Proteins↗
PubMed2005

Activity-guided identification of (S)-malic acid 1-O-D-glucopyranoside (morelid) and gamma-aminobutyric acid as contributors to umami taste and mouth-drying oral sensation of morel mushrooms (Morchella deliciosa Fr.).

Although morel mushrooms are widely used as tasty ingredients in savory dishes, knowledge of the key compounds evoking their attractive taste is still very fragmentary. In the present study, taste activity-guided fractionation of an aqueous morel extract by means of the recently developed taste dilution analysis (TDA) enabled the localization of several umami-like-tasting fractions as well as a fraction imparting an intense mouth-drying sensation to the oral cavity. Hydrophilic interaction liquid chromatography (HILIC), LC-MS, and amino acid analysis led to the successful identification of gamma-aminobutyric acid as the chemical inducer of the mouth-drying and mouth-coating oral sensations imparted by the morel extract. Besides the well-known umami-like taste contributors L-glutamic acid, L-aspartic acid, and succinic acid, an additional HILIC fraction was isolated and evaluated as tasting umami-like. LC-MS and NMR studies revealed that this fraction consisted of a mixture of (S)-malic acid 1-O-alpha-D-glucopyranoside and (S)-malic acid 1-O-beta-D-glucopyranoside, the structure of which could be successfully confirmed by independent synthesis. To the best of our knowledge, this morel-derived glycoside, which we named (S)-morelid, has previously not been reported in any food products. Sensory analysis of aqueous solutions of the compounds identified revealed threshold concentrations of 0.02 mmol/L for the mouth-drying effect of gamma-aminobutyric acid and 6.0 mmol/L for the umami-like, slightly sour taste of (S)-morelid.

Ascomycota↗
PubMed2002

Action of 4-amino-2-fluorobutanoic acid and other structural analogues on gamma-aminobutyric acid transport by channel catfish brain.

Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in mammalian brain. The synaptic action of GABA is terminated by a sodium- and chloride-linked transport system. The GABA transporter is known as GAT and several isoforms have been identified. Many components of a GABA neurotransmitter system, including a GABA transport system, are present in channel catfish brain. Using a synaptosomal preparation of catfish brain, we examined the kinetics of inhibition of GABA transport by 4-amino-2-fluorobutanoic acid and several other structural analogues of GABA. The transport constant (Kt) for GABA uptake was 4.46 microM, and 4-amino-2-fluorobutanoic acid produced a noncompetitive type of inhibition (Ki = 12.5 microM). The most potent inhibitors were tiagabine (Ki = 0.23 microM) and (R,S)nipecotic acid (Ki = 2.2 microM), both of which exhibited competitive inhibition. Like 4-amino-2-fluorobutanoic acid, homo-beta-proline (Ki = 9.4 microM) inhibited noncompetitively. Other analogues exhibited competitive inhibition. These observations suggest that the GABA transport system in channel catfish is remarkably similar to that in mammalian brain.

Animals↗
PubMed1982

[Release of gamma-aminobutyric acid from cat colon].

The release of gamma-aminobutyric acid was confirmed in isolated cat colon loaded with tritiated gamma-aminobutyric acid. Thirty to 180 minutes after loading the spontaneous efflux of tritium appeared to fit a single exponential curve with an efflux rate coefficient of 0.002 per minute. Electrical stimulation produced frequency-dependent increases in the tritium efflux and in the contractions. Even 120 minutes later over 91 percent of the total radioactivity in the superfusates was attributable to tritiated gamma-aminobutyric acid. The acid release and the contractions induced by electrical transmural stimulation were inhibited by tetrodotoxin and by a calcium-free medium. Release of the acid was not significant during contractions elicited by nicotine and acetylcholine. These findings indicate that gamma-aminobutyric acid is released from the terminals of neurons in the myenteric plexus of the colon.

Acetylcholine↗
PubMed1975

Effect of hashish on brain gamma aminobutyric acid system, blood fibrinolytic activity and glucose and some serum enzymes in the rat.

Adult male rats were exposed to Hashish smoke for 15 min. Certain biochemical parameters were determined. This treatment did not change the brain glutamic acid level, whereas it significantly decreased brain gamma aminobutyric acid level. There was a significant increase in the activity of the brain enzyme forming gamma aminobutyric acid, namely glutamate decarboxylase, as well as in that enzyme metabolizing gamma aminobutyric acid, namely aminobutyrate aminotransferase. However, the increase was much more marked in the case of aminobutyrate aminotransferase, a finding that might explain the decrease observed in brain gamma aminobutyric acid upon exposure to Hashish. Blood glucose and fibrinolytic activity were significantly increased. It was concluded that these changes might be due to an adrenaline releasing effect of Hashish smoke inhalation. Serum lactate dehydrogenase and serum glutamate oxalacetate transaminase activities were significantly increased, whereas serum glutamate pyruvate transaminase activity was unaffected. From these data it was suggested that the source of leakage of these enzyme activities into the blood is probably the skeletal muscles rather than the liver.

4-Aminobutyrate Transaminase↗
PubMed1994

Identification of tryptophan residues critical for the function and targeting of the gamma-aminobutyric acid transporter (subtype A).

The gamma-aminobutyric acid transporter is localized in nerve terminals. It catalyzes coupled electrogenic translocation of the neurotransmitter with two or three sodium ions and one chloride ion. The transporter contains 599 amino acids and 12 putative membrane spanning alpha-helices. It is the first described member of a neurotransmitter transporter superfamily. Using site-directed mutagenesis we have investigated the role of all 10 tryptophan residues predicted to reside in these helices. All 10 have been changed to serine as well as to leucine residues. Expression of mutant cDNAs in which the tryptophans, located in positions 68, 222, and 230, are replaced by either of these two amino acids reveals that they are severely impaired in gamma-aminobutyric acid transport. Mutants in which a phenylalanine or a tyrosine residue is introduced, at either position 68 or 230, are active. On the other hand, at the 222 position replacement of the tryptophan by the aromatic amino acids results in inactive transport. After prelabeling of the proteins with [35S]methionine, immunoprecipitation of mutant transporters indicates that their expression levels are similar to those of the wild type. Reconstitution experiments, aimed to reveal the activity of transporter molecules not apparent in the plasma membrane, indicate that the lack of activity of the W230S transporter in intact cells is by and large due to its inefficient targeting to the plasma membrane. Tryptophan residues 68 and 222 appear to be required for the intrinsic activity of the transporter. Based on several observations, including one that tryptophan residue 222 is conserved in all amino acid transporter members of the superfamily, but not in those transporting biogenic amines, we hypothesize that the pi electrons of this tryptophan could be involved in the binding of the amino group of these neurotransmitters.

Amino Acid Sequence↗
PubMed1987

Brain gamma-aminobutyric acid receptor binding is normal in rats with thioacetamide-induced hepatic encephalopathy despite elevated plasma gamma-aminobutyric acid-like activity.

Brain gamma-aminobutyric acid (GABA) receptor density, affinity, and function, and plasma GABA-like activity were determined in rats with acute hepatic encephalopathy induced by an intraperitoneal injection of thioacetamide. In addition, the effect of various stress factors on brain GABA binding was assessed. Plasma GABA-like activity was significantly increased in rats with thioacetamide-induced hepatic encephalopathy compared with rats injected with vehicle alone (1506 +/- 993 nM, n = 7 vs. 367 +/- 97 nM, n = 9, mean +/- SD; p less than 0.001). In contrast, there were no alterations in either brain GABA receptor binding or in GABA-enhanced benzodiazepine binding in rats with hepatic encephalopathy when compared with relevant controls. However, rats that had received intraperitoneal injections of thioacetamide or vehicle (0.15 M NaCl) had significantly more low-affinity GABA receptors than rats that had neither been injected nor handled before killing (8769 +/- 1101 vs. 2710 +/- 757 fmol/mg protein, mean +/- SEM, p less than 0.001). We concluded that stress factors appear to be important causes of altered brain GABA binding. Brain GABA receptor binding and function, however, are unaltered in rats with thioacetamide-induced hepatic encephalopathy despite elevated plasma GABA-like activity.

Animals↗
PubMed1991

Peripheral projections of the chick primary sensory neurons expressing gamma-aminobutyric acid immunoreactivity.

The expression of gamma-aminobutyric acid was studied in sensory neurons and peripheral target tissues of the chick dorsal root ganglia by combining immunocytochemistry and electron microscopy. In the chick embryos, the first immunoreaction was observed at embryonic day 12 in 1.4% of ganglion cell bodies. The intensity of immunostaining gradually increased during development and the percentage of immunostained neurons reached an average of 7.3% after hatching. These immunostained cell bodies could be identified as sensory neurons belonging either to some large neurons of the A1 subclass or to a few small neurons of the B1 subclass. The other neuronal cell bodies, corresponding to the A2 and B2 subclasses, as well as the satellite and glial cells were apparently devoid of any gamma-aminobutyric acid immunostaining. Among the peripheral tissues innervated by the primary sensory neurons, the nerve endings of Achilles' tendon and the paravertebral autonomic ganglia appeared devoid of immunoreactivity. In contrast, immunoreactivity was found within nerve endings located in some neuromuscular spindles of the skeletal muscles and within some Herbst's corpuscles in the subcutaneous tissue of the skin. Thus, the present results provide evidence that gamma-aminobutyric acid may be expressed by neuronal cell bodies belonging to two subclasses of primary sensory neurons and could be a putative neurotransmitter involved in the peripheral sensory innervation of, at least in part, skin and skeletal muscles.

Animals↗
PubMedDate not supplied

Effects of melatonin on hypothalamic gamma-aminobutyric acid, aspartic acid, glutamic acid, beta-endorphin and serotonin levels in male mice.

Effects of melatonin on hypothalamic neurotransmitters in male mice were studied. Exogenous melatonin administered intraperitoneally significantly increased (p < 0.05) hypothalamic concentrations of aspartic acid and gamma-aminobutyric acid by over 29 and 50% respectively. Conversely, hypothalamic beta-endorphin concentration was significantly decreased (p < 0.05) 30 min after melatonin administration with doses between 5- and 100 micrograms/kg. Similarly, melatonin, at a concentration of 100 micrograms/kg, decreased (p < 0.05) the serotonin level in mouse hypothalamus by 46%. Melatonin, however, did not affect the concentration of hypothalamic glutamic acid over a dose range of 0.5-300 micrograms melatonin/kg. Our findings suggested that actions of pineal melatonin in animals such as inhibition on serum corticosterone levels might be mediated by the potentiation of activities of hypothalamic neurons containing gamma-aminobutyric acid and aspartic acid or by the inhibition of the beta-endorphin and serotonin hypothalamic neurons. The neurons containing glutamic acid in the hypothalamus were, however, not influenced by melatonin. Our results are in line with the suggestion that melatonin actions on adrenal corticosterone release or other endocrine secretions may be mediated by way of its actions on hypothalamic neurotransmitter activities.

Animals↗
PubMed1980

Regional distributions of gamma-aminobutyric acid (GABA), glutamate decarboxylase (GAD), and gamma-aminobutyrate transaminase (GABA-T) in the central nervous brains of C57/BR, C3H/He, and F1 hybrid mice.

The distributions of gamma-aminobutyric acid (GABA), glutamate decarboxylase (GAD), and gamma-aminobutyrate transaminase (GABA-T) have been studied in various brain areas of mice. These neurochemical markers, which are related to inhibitory neurotransmission, were investigated in different inbred strains of mice (C3H/He, C57/BR, and their F1 hybrids). The regional distributions of GABA, GAD activity, and GABA-T activity in adult mice of these three strains were quite similar. No significant differences were found in any brain area for GAD or GABA-T activity. However, significant differences in GABA level were found in several brain areas among these strains of mice, especially in hypothalamus, hippocampus, olfactory bulb, and occipital cortex. These results provide further information to the possible influence of the GABAergic system in these brain areas.

4-Aminobutyrate Transaminase↗