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| β-Alanine (beta-alanine) is a naturally occurring beta amino acid, which is an amino acid in which the amino group is attached to the β-carbon (i.e. the carbon two carbon atoms away from the carboxylate group) instead of the more usual α-carbon for alanine (α-alanine). The IUPAC name for β-alanine is 3-aminopropanoic acid. Unlike its counterpart α-alanine, β-alanine has no stereocenter.
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Read full article at Wikipedia
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| InChI=1S/C3H7NO2/c4-2-1-3(5)6/h1-2,4H2,(H,5,6) |
| UCMIRNVEIXFBKS-UHFFFAOYSA-N |
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Saccharomyces cerevisiae
(NCBI:txid4932)
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Source: yeast.sf.net
See:
PubMed
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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Bronsted base
A molecular entity capable of accepting a hydron from a donor (Bronsted acid).
(via organic amino compound )
Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via oxoacid )
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human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
fundamental metabolite
Any metabolite produced by all living cells.
inhibitor
A substance that diminishes the rate of a chemical reaction.
agonist
Substance which binds to cell receptors normally responding to naturally occurring substances and which produces a response of its own.
neurotransmitter
An endogenous compound that is used to transmit information across the synapse between a neuron and another cell.
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View more via ChEBI Ontology
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3-aminopropanoic acid
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β-alanine
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3-aminopropanoic acid
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ChEBI
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3-Aminopropionic acid
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KEGG COMPOUND
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bAla
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ChEBI
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beta-Alanine
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KEGG COMPOUND
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BETA-ALANINE
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PDBeChem
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β-aminopropionic acid
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NIST Chemistry WebBook
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H-β-Ala-OH
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ChEBI
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ω-aminopropionic acid
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ChEBI
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107-95-9
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CAS Registry Number
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KEGG COMPOUND
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107-95-9
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CAS Registry Number
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ChemIDplus
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107-95-9
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CAS Registry Number
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NIST Chemistry WebBook
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49614
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Gmelin Registry Number
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Gmelin
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906793
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Reaxys Registry Number
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Reaxys
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Bordbar A, Mo ML, Nakayasu ES, Schrimpe-Rutledge AC, Kim YM, Metz TO, Jones MB, Frank BC, Smith RD, Peterson SN, Hyduke DR, Adkins JN, Palsson BO (2012)
Model-driven multi-omic data analysis elucidates metabolic immunomodulators of macrophage activation.
Molecular systems biology 8, 558 [PubMed:22735334]
[show Abstract]
Macrophages are central players in immune response, manifesting divergent phenotypes to control inflammation and innate immunity through release of cytokines and other signaling factors. Recently, the focus on metabolism has been reemphasized as critical signaling and regulatory pathways of human pathophysiology, ranging from cancer to aging, often converge on metabolic responses. Here, we used genome-scale modeling and multi-omics (transcriptomics, proteomics, and metabolomics) analysis to assess metabolic features that are critical for macrophage activation. We constructed a genome-scale metabolic network for the RAW 264.7 cell line to determine metabolic modulators of activation. Metabolites well-known to be associated with immunoactivation (glucose and arginine) and immunosuppression (tryptophan and vitamin D3) were among the most critical effectors. Intracellular metabolic mechanisms were assessed, identifying a suppressive role for de-novo nucleotide synthesis. Finally, underlying metabolic mechanisms of macrophage activation are identified by analyzing multi-omic data obtained from LPS-stimulated RAW cells in the context of our flux-based predictions. Our study demonstrates metabolism's role in regulating activation may be greater than previously anticipated and elucidates underlying connections between activation and metabolic effectors. | Walter AA, Smith AE, Kendall KL, Kendall KL, Stout JR, Cramer JT (2010)
Six weeks of high-intensity interval training with and without beta-alanine supplementation for improving cardiovascular fitness in women.
Journal of strength and conditioning research 24, 1199-1207 [PubMed:20386120]
[show Abstract]
The purpose of the present study was to evaluate the effects of cycle ergometry high-intensity interval training (HIIT) with and without beta-alanine supplementation on maximal oxygen consumption rate (VO2 peak), cycle ergometer workload at the ventilatory threshold (VT W), and body composition. Forty-four women (mean +/- SD age = 21.8 +/- 3.7 years; height = 166.5 +/- 6.6 cm; body mass (BM) = 65.9 +/- 10.8 kg; VO2 peak = 31.5 +/- 6.2 ml x kg(-1) x min(-1)) were randomly assigned to 1 of 3 groups: beta-alanine (BA, n = 14) 1.5 g + 15 g dextrose powder; placebo (PL, n = 19) 16.5 g dextrose powder; or control (CON, n = 11). Testing was conducted at baseline (week 0), after 3 weeks (week 4), and after 6 weeks (week 8). VO2 peak (ml x kg(-1) x min(-1)) and VT W were measured with a metabolic cart during graded exercise tests on a corival cycle ergometer, and body composition (percent fat = % fat and fat-free mass = FFM) were determined by air displacement plethysmography. High-intensity interval training was performed on a corival cycle ergometer 3 times per week with 5 2-minute work intervals and 1-minute passive recovery with undulating intensities (90-110% of the workload recorded at VO2 peak) during each training session. VO2 peak increased (p 0.05) for the CON group. VT W increased (p | Artioli GG, Gualano B, Smith A, Stout J, Lancha AH (2010)
Role of beta-alanine supplementation on muscle carnosine and exercise performance.
Medicine and science in sports and exercise 42, 1162-1173 [PubMed:20479615]
[show Abstract]
In this narrative review, we present and discuss the current knowledge available on carnosine and beta-alanine metabolism as well as the effects of beta-alanine supplementation on exercise performance. Intramuscular acidosis has been attributed to be one of the main causes of fatigue during intense exercise. Carnosine has been shown to play a significant role in muscle pH regulation. Carnosine is synthesized in skeletal muscle from the amino acids l-histidine and beta-alanine. The rate-limiting factor of carnosine synthesis is beta-alanine availability. Supplementation with beta-alanine has been shown to increase muscle carnosine content and therefore total muscle buffer capacity, with the potential to elicit improvements in physical performance during high-intensity exercise. Studies on beta-alanine supplementation and exercise performance have demonstrated improvements in performance during multiple bouts of high-intensity exercise and in single bouts of exercise lasting more than 60 s. Similarly, beta-alanine supplementation has been shown to delay the onset of neuromuscular fatigue. Although beta-alanine does not improve maximal strength or VO2max, some aspects of endurance performance, such as anaerobic threshold and time to exhaustion, can be enhanced. Symptoms of paresthesia may be observed if a single dose higher than 800 mg is ingested. The symptoms, however, are transient and related to the increase in plasma concentration. They can be prevented by using controlled release capsules and smaller dosing strategies. No important side effect was related to the use of this amino acid so far. In conclusion, beta-alanine supplementation seems to be a safe nutritional strategy capable of improving high-intensity anaerobic performance. | Derave W, Everaert I, Beeckman S, Baguet A (2010)
Muscle carnosine metabolism and beta-alanine supplementation in relation to exercise and training.
Sports medicine (Auckland, N.Z.) 40, 247-263 [PubMed:20199122]
[show Abstract]
Carnosine is a dipeptide with a high concentration in mammalian skeletal muscle. It is synthesized by carnosine synthase from the amino acids L-histidine and beta-alanine, of which the latter is the rate-limiting precursor, and degraded by carnosinase. Recent studies have shown that the chronic oral ingestion of beta-alanine can substantially elevate (up to 80%) the carnosine content of human skeletal muscle. Interestingly, muscle carnosine loading leads to improved performance in high-intensity exercise in both untrained and trained individuals. Although carnosine is not involved in the classic adenosine triphosphate-generating metabolic pathways, this suggests an important role of the dipeptide in the homeostasis of contracting muscle cells, especially during high rates of anaerobic energy delivery. Carnosine may attenuate acidosis by acting as a pH buffer, but improved contractile performance may also be obtained by improved excitation-contraction coupling and defence against reactive oxygen species. High carnosine concentrations are found in individuals with a high proportion of fast-twitch fibres, because these fibres are enriched with the dipeptide. Muscle carnosine content is lower in women, declines with age and is probably lower in vegetarians, whose diets are deprived of beta-alanine. Sprint-trained athletes display markedly high muscular carnosine, but the acute effect of several weeks of training on muscle carnosine is limited. High carnosine levels in elite sprinters are therefore either an important genetically determined talent selection criterion or a result of slow adaptation to years of training. beta-Alanine is rapidly developing as a popular ergogenic nutritional supplement for athletes worldwide, and the currently available scientific literature suggests that its use is evidence based. However, many aspects of the supplement, such as the potential side effects and the mechanism of action, require additional and thorough investigation by the sports science community. | Takahashi K, Azuma Y, Kobayashi S, Azuma J, Takahashi K, Schaffer SW, Hattori M, Namba T (2009)
Tool from traditional medicines is useful for health-medication: Bezoar Bovis and taurine.
Advances in experimental medicine and biology 643, 95-103 [PubMed:19239140]
[show Abstract]
Bezoar Bovis (BB:dried cattle gallbladder stones) has been used empirically in Asia for over 3000 years to treat heart and liver disorders. Yet its therapeutic potential remains unexplored by Western researchers. The aim of this study has been to clarify the actions of BB on cultured cardiomyocytes and to identify its active component(s). BB is a component of 98.7% of the Japanese over the counter (OTC) cardioactive drugs. The water-extract of BB exhibits protection action against arrhythmias produced by low Ca2+ and high Ca2+ in the medium. On the other hand, the Ca(2+)-antagonist, verapamil, did not suppress arrhythmias that developed in cell culture. Rather, it aggravated the beating status of the cardiomyocytes. The major constituents of the BB extract are bile salts (cholate, deoxycholate, taurocholate) and amino acids (taurine, cysteine, leucine, isoleucine). Most cells incubated with bile salts developed morphological damage. However, one of the major constituents of the BB extract, taurine, was effective in protecting against the abnormal beating pattern induced by high Ca2+. Since beta-alanine, an inhibitor of taurine transport, antagonized the protective effects of both BB and taurine, it is likely that the effect of BB is partly mediated by taurine. | Inoue K, Karashima T, Kamada M, Shuin T, Kurabayashi A, Furihata M, Fujita H, Utsumi K, Sasaki J (2009)
Regulation of 5-aminolevulinic acid-mediated protoporphyrin IX accumulation in human urothelial carcinomas.
Pathobiology : journal of immunopathology, molecular and cellular biology 76, 303-314 [PubMed:19955842]
[show Abstract]
PurposeThe purpose of this study was to clarify the regulatory mechanism of protoporphyrin IX (PpIX) synthesis mediated by 5-aminolevulinic acid (ALA) in human urothelial carcinoma (UC), leading to improved accuracy in photodynamic diagnosis and therapy using ALA.Experimental designPpIX accumulation in cultured UC cells after incubation for 1-5 h with 0.5-5 mM ALA was analyzed by fluorescence analysis using fluorescence microscopy and flow cytometry technique.ResultsPpIX fluorescence mediated by ALA was increased, and the intensity of PpIX fluorescence was time-dependently increased in UC cells compared to noncancerous cells. The distribution of endogenous PpIX fluorescence primarily coincided with mitochondria, and then increased at a specific perinuclear region in the cells during the time of incubation. The ALA-mediated PpIX synthesis in UC cells was suppressed by beta-alanine, an inhibitor of beta-transporters of cell membrane, and carbonylcyanide p-trifluoromethoxyphenyl hydrazone, an uncoupler of mitochondrial oxidative phosphorylation. In contrast, the ALA-mediated PpIX accumulation was increased by deferoxamine, an iron chelator, manganese and nitric oxide, which is contributed to PpIX metabolism by inhibiting ferrochelatase activity, generated by a nitric oxide-generating reagent NOC-18. As observed above, ALA-mediated PpIX synthesis in human UC cells was regulated by the process of ALA uptake, ALA conversion to PpIX and metabolism of accumulated PpIX to heme.ConclusionsThis shows that the suppression of ferrochelatase increased PpIX accumulation in UC cells using small amount of ALA, thus leading to an improved clinical practicability of photodynamic diagnosis and therapy. | Krylova LF, Kovtunova LM, Romanenko GV (2008)
Pt(II) and Pd(II) complexes with beta-alanine.
Bioinorganic chemistry and applications983725 [PubMed:18528519]
[show Abstract]
A sequence of stages in the syntheses of isomeric bisamino acid complexes of Pt(II) with beta-aminopropionic acid (beta-alanine = beta-AlaH) has been studied by the (195)Pt NMR spectroscopy. The techniques have been developed of the synthesis of the cis- and trans-bischelates of Pt(II) and Pd(II) with beta-alanine as well as of the halide complexes of trans-[M(beta-AlaH)(2)Cl(2)] (M = Pt, Pd) and trans-K(2)[Pt(beta-Ala)(2)I(2)] types. The NMR spectroscopy and IR spectroscopy (in the nuclei of (195)Pt,(13)C,(1)H) and X-ray diffraction analysis have been used to examine the structures of the synthesized compounds. | Hannestad U, Theodorsson E, Evengård B (2007)
beta-Alanine and gamma-aminobutyric acid in chronic fatigue syndrome.
Clinica chimica acta; international journal of clinical chemistry 376, 23-29 [PubMed:16934791]
[show Abstract]
BackgroundDue to the occurrence of sleep disturbances and fatigue in chronic fatigue syndrome (CFS), an investigation was performed to examine if there is an abnormal excretion of gamma-aminobutyric acid (GABA) and/or its structural analogue beta-alanine in the urine from CFS patients. Both GABA and beta-alanine are inhibitory neurotransmitters in the mammalian central nervous system.MethodsThe 24 h urine excretion of GABA and beta-alanine was determined by isotope dilution gas chromatography mass spectrometry in 33 CFS patients and 43 healthy controls. The degree of symptoms in both patients and controls was measured by grading of three typical CFS symptoms using a Visual Analogue Scale.ResultsMen had a significantly higher excretion of both beta-alanine and GABA than women. Comparing CFS patients with healthy controls showed no significant difference in excretion of neither beta-alanine nor GABA. No correlation was found between the excretion of beta-alanine or GABA and any of the three characteristic CFS symptoms measured. However, two female and two male CFS patients excreted considerably higher amounts of beta-alanine in their 24 h urine samples than control subjects.ConclusionsIncreased excretion of beta-alanine was found in a subgroup of CFS patients, indicating that there may be a link between CFS and beta-alanine in some CFS patients. | Okimura Y, Fujita H, Ogino T, Inoue K, Shuin T, Yano H, Yasuda T, Inoue M, Utsumi K, Sasaki J (2007)
Regulation of 5-aminolevulinic acid-dependent protoporphyrin IX accumulations in human histiocytic lymphoma U937 cells.
Physiological chemistry and physics and medical NMR 39, 69-82 [PubMed:18613640]
[show Abstract]
The aim of the present work is to clarify the mechanism(s) that regulates the accumulation of protoporphyrin IX (PpIX) in human histiocytic lymphoma cell line U937 incubated with 5-aminolevulinic acid (ALA). Biosynthesis and accumulation of PpIX in the cells was determined after incubation with 0.1-5 mM ALA using a flow cytometric technique. The synthesized endogenous PpIX was found to localize predominantly in the mitochondrial region of the cells. The ALA-enhanced PpIX synthesis was suppressed by the presence of either beta-alanine, a competitive inhibitor of beta-transporters on cell membranes, or carbonyl cyanide p-trifluoromethoxyphenyl hydrazone, an uncoupler of mitochondrial oxidative phosphorylation. In contrast, cellular accumulation of PpIX was enhanced by the presence of either deferoxamine (an iron chelater), MnCl2 (a ferrochelatase inhibitor), or Sn-mesoporphyrin (heme oxygenase inhibitor). These results suggest that ALA-enhanced accumulation of PpIX in U937 cells was regulated by cellular uptake and conversion of ALA to PpIX and by degradation of Heme. | González-Quevedo A, Obregón F, Urbina M, Roussó T, Lima L (2003)
Effects of taurine deficiency and chronic methanol administration on rat retina, optic nerve and brain amino acids and monoamines.
Nutritional neuroscience 6, 253-261 [PubMed:12887142]
[show Abstract]
A chronic methanol (MeOH) intoxication scheme (2 g/kg/day ip for 2 weeks) was carried out in Sprague-Dawley rats, previously depleted of folates with methotrexate (MTX). beta-Alanine (beta-Ala), 5%, was also administered to some animals in the drinking water. Amino acids were determined in plasma, retina, optic nerve, hippocampus and posterior cortex by HPLC with fluorescence detection and monoamines in retina, hippocampus and posterior cortex by electrochemical detection. Beta-Ala administration reduced taurine (Tau) levels in plasma, hippocampus and posterior cortex, but not in retina and optic nerve. Aspartate (Asp) concentration in the optic nerve was increased in MTX-MeOH treated animals, and the administration of beta-Ala did not modify this elevation. The association of beta-Ala with MTX-MeOH produced an increase of threonine, and a decrease of 5-hydroxytryptamine (5-HT) in the retina without modifying 5-hydroxyindoleacetic acid, whereas in the hippocampus an elevation of asparagine was observed. We conclude that, in the retina, beta-Ala in combination with MTX-MeOH increased serotonin and decreased dopamine (DA) turnover rate, and resulted in changes in the amino acid balance, that could affect glycinergic activity. On the other hand, in the hippocampus, Asp metabolism could be affected by Tau depletion with beta-Ala. | Dawson R, Biasetti M, Messina S, Dominy J (2002)
The cytoprotective role of taurine in exercise-induced muscle injury.
Amino acids 22, 309-324 [PubMed:12107759]
[show Abstract]
Intense exercise is thought to increase oxidative stress and damage muscle tissue. Taurine is present in high concentration in skeletal muscle and may play a role in cellular defenses against free radical-mediated damage. The aim of this study was to determine if manipulating muscle levels of taurine would alter markers of free radical damage after exercise-induced injury. Adult male Sprague-Dawley rats were supplemented via the drinking water with either 3% (w/v) taurine (n = 10) or the competitive taurine transport inhibitor, beta-alanine (n = 10), for one month. Controls (n = 20) drank tap water containing 0.02% taurine and all rats were placed on a taurine free diet. All the rats except one group of sedentary controls (n = 10) were subjected to 90 minutes of downhill treadmill running. Markers of cellular injury and free radical damage were determined along with tissue amino acid content. The 3% taurine treatment raised plasma levels about 2-fold and 3% beta-alanine reduced plasma taurine levels about 50%. Taurine supplementation (TS) significantly increased plasma glutamate levels in exercised rats. Exercise reduced plasma methionine levels and taurine prevented its decline. Taurine supplementation increased muscle taurine content significantly in all muscles except the soleus. beta-alanine decreased muscle taurine content about 50% in all the muscles examined. Lipid peroxidation (TBARS) was significantly increased by exercise in the extensor digitorium longus (EDL) and gastrocnemius (GAST) muscles. Both taurine and beta-alanine completely blocked the increase in TBARs in the EDL, but had no effect in the GAST. Muscle content of the cytosolic enzyme, lactate dehydrogenase (LDH) was significantly decreased by exercise in the GAST muscle and this effect was attenuated by both taurine and beta-alanine. Muscle myeloperoxidase (MPO) activity was significantly elevated in the gastrocnemius muscle, but diet had no effect. MPO activity was significantly increased by exercise in the liver and both taurine and beta-alanine blocked this effect. There was no effect of either exercise or the diets on MPO activity in the lung or spleen. Running performance as assessed by a subjective rating scale was improved by taurine supplementation and there was a significant loss in body weight in the beta-alanine-treated rats 24 hours after exercise. In summary, taurine supplementation or taurine depletion had measurable cytoprotective actions to attenuate exercise-induced injury. | Mori M, Gähwiler BH, Gerber U (2002)
Beta-alanine and taurine as endogenous agonists at glycine receptors in rat hippocampus in vitro.
The Journal of physiology 539, 191-200 [PubMed:11850512]
[show Abstract]
Electrophysiological and pharmacological properties of glycine receptors were characterized in hippocampal organotypic slice cultures. In the presence of ionotropic glutamate and GABA(B) receptor antagonists, pressure-application of glycine onto CA3 pyramidal cells induced a current associated with increased chloride conductance, which was inhibited by strychnine. Similar chloride currents could also be induced with beta-alanine or taurine. Whole-cell glycine responses were significantly greater in CA3 pyramidal cells than in CA1 pyramidal cells and dentate granule cells, while responses to GABA were similar among these three cell types. Although these results demonstrate the presence of functional glycine receptors in the hippocampus, no evidence for their activation during synaptic stimulation was found. Gabazine, a selective GABA(A) receptor antagonist, totally blocked evoked IPSCs in CA3 pyramidal cells. Glycine receptor activation is not dependent on transporter-controlled levels of extracellular glycine, as no chloride current was observed in response to sarcosine, an inhibitor of glycine transporters. In contrast, application of guanidinoethanesulfonic acid, an uptake inhibitor of beta-alanine and taurine, induced strychnine-sensitive chloride current in the presence of gabazine. These data indicate that modulation of transporters for the endogenous amino acids, beta-alanine and taurine, can regulate tonic activation of glycine receptors, which may function in maintenance of inhibitory tone in the hippocampus. | Llanos MN, Ronco AM, Aguirre MC, Meizel S (2001)
Hamster sperm glycine receptor: evidence for its presence and involvement in the acrosome reaction.
Molecular reproduction and development 58, 205-215 [PubMed:11139233]
[show Abstract]
Recent reports have provided evidence for the presence of amino acid neurotransmitter receptor/chloride channels in human and porcine spermatozoa and their involvement in the acrosome reaction (AR). In this work we investigated whether a glycine receptor (GlyR) was present in golden hamster sperm, and whether it had a role in the hamster AR. The neuronal GlyR agonist glycine, stimulated in a dose-dependent manner, the AR of hamster spermatozoa previously capacitated for at least 3 hr. This stimulation was completely inhibited by 50 microM (+)-bicuculline and by concentrations of strychnine as low as 10-50 nM; both agents are antagonists of neuronal GlyR when used at the concentrations reported in this study. beta-Alanine, another agonist of the neuronal GlyR, also stimulated the AR. The AR-stimulatory effect of this compound was completely abolished by 50 nM strychnine. The inhibitory effect of strychnine on the glycine-induced hamster sperm AR was completely overcome by subsequent treatment with the calcium ionophore ionomycin, demonstrating that the strychnine effect was specific for GlyR. Additional binding studies with (3)[H]-strychnine, the typical radioligand used to detect GlyR in several cells, demonstrated for the first time the presence of specific binding sites for strychnine in the hamster spermatozoa. Interestingly, binding increased during in vitro capacitation, particularly in those sperm suspensions showing high percentages of AR. Taken together these results strongly suggest the presence of a GlyR in the hamster spermatozoa, with a role in the AR when activated. | JONES NR (1955)
The free amino acids of fish; 1-methylhistidine and beta-alanine liberation by skeletal muscle anserinase of codling (Gadus callarias).
The Biochemical journal 60, 81-87 [PubMed:14363188] | KING JA, McMILLAN FH (1946)
The preparation and properties of some beta-aminopropionic acid derivatives.
Journal of the American Chemical Society 68, 1468-1470 [PubMed:20994958] |
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