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PubMed1978

Action of glutamic acid and of some glutamate analogues on the molluscan central neurones.

The effects of L-glutamic acid and of some glutamate analogues have been studied on the central nervous system of the snail Heobania vermiculata, using conventional electrophysiological techniques. The glutamate H-response had the mean equilibrium value of -(57 +/- 4) mV and was associated with a Cl- conductance change. The D-response to glutamate application showed an involvement of sodium ions. Aspartate was agonist of glutamate action and displayed similar equilibrium value of the H-response, whereas quisqualate H-response was 'non-invertible'.

Animals↗
PubMed2002

GltS, the sodium-coupled L-glutamate uptake system of Corynebacterium glutamicum: identification of the corresponding gene and impact on L-glutamate production.

A screening procedure was established to identify Corynebacterium glutamicum transposon mutants with an altered L-glutamate excretion behaviour. By this microtiter plate-based approach seven non- or less excreting C. glutamicum strains and two hyper-excreters were found. The subsequently carried out molecular analysis of a hyper-producing clone led to the identification of the gltS gene, which codes for the sodium-coupled secondary L-glutamate uptake system in C. glutamicum. Characterization of a gltS deletion strain revealed that this transporter has a weak but significant impact on L-glutamate production induced by biotin limitation in the wild type. Obviously, GltS leads to the re-uptake of excreted L-glutamate causing a futile cycle. In accord with this hypothesis, the overexpression of gltS decreased L-glutamate production.

Amino Acid Transport Systems, Acidic↗
PubMed2005

A metal ion as a cofactor attenuates substrate inhibition in the enzymatic production of a high concentration of D-glutamate using N-acyl-D-glutamate amidohydrolase.

N-Acyl-D-glutamate amidohydrolase (D-AGase) was inhibited by 94 % when 1 mol/l N-acetyl-DL-glutamate was used as a substrate. The addition of 1 mM Co2+ stabilized D-AGase. Moreover, the substrate inhibition was weakened to 88% with the addition of 0.4 mM Co2+ to the reaction mixture. Although D-AGase is a zinc-metalloenzyme, the addition of Zn2+ from 0.01 to 10 mM did not increase the D-glutamic acid production in the saturated substrate. Under optimal conditions, 0.38 M D-glutamic acid was obtained from N-acyl-DL-glutamate with 100% of the theoretical yield after 48 h.

Alcaligenes↗
PubMed2004

Glutamate regulates the frequency of spontaneous synchronized Ca2+ spikes through group II metabotropic glutamate receptor in cultured mouse cortical networks.

1. Synchronized spontaneous intracellular Ca2+ spikes in networked neurons are believed to play a major role in the development and plasticity of neural circuits. Glutamate-induced signals through the ionotropic glutamate receptors (iGluRs) are profoundly involved in the generation of synchronized Ca2+ spikes. 2. In this study, we examined the involvement of metabotropic glutamate receptors (mGluRs) in cultured mouse cortical neurons. We pharmacologically revealed that glutamate-induced signals through inclusive mGluRs decreased the frequency of Ca2+ spikes. Further experiments indicated that this suppressive effect on the spike frequency was mainly due to the signal through group II mGluR, inactivation of adenylate cyclase-cAMP-PKA signaling pathway. Group I mGluR had little involvement in the spike frequency. 3. Taken together, glutamate generates the synchronized Ca2+ spikes through iGluRs and modulates simultaneously their frequency through group II mGluR-adenylate cyclase-cAMP-PKA signaling pathway in the present in vitro neural network. These results provide the evidence of the profound role of group II mGluR in the spontaneous and synchronous neural activities.

Action Potentials↗
PubMed1976

Antagonism of cortical excitation of striatal neurons by glutamic acid diethyl ester: evidence for glutamic acid as an excitatory transmitter in the rat striatum.

Rat striatal cells that were excited by cortical stimulation were found to respond to cortical stimulation with an average latency of 12 msec. Each response consisted of a variable number of spikes with, on the average, a less than 1:1 relationship between the stimulus and the number of spikes generated. Iontophoretic application of glutamic acid diethyl ester (GDEE), a substance reported to be a glutamate antagonist, at currents of +50 to +125 nA in the vicinity of neurons exicted by cortical stimulation, almost totally suppressed the excitation in 90% of the cells, and this suppression was fully reversible. All cells were excited by glutamate. GDEE also suppressed neuronal excitation produced by iontophoretic aspartate, glutamate and DL-homocysteic acid. It is concluded from this study that an excitatory amino acid, either aspartic or glutamic, may function as the transmitter in the corticostriate projection.

Animals↗
PubMed1990

Amiloride blocks glutamate-operated cationic channels and protects neurons in culture from glutamate-induced death.

The diuretic amiloride has been suggested as a specific inhibitor of T-type neuronal Ca2+ channels. The effects of amiloride on glutamate receptor-gated cationic channels and glutamate-induced. Ca2(+)-dependent neuronal death were investigated in primary neuronal cultures from neonatal rats. In primary cultures of cerebellar granule neurons of the rat, receiving 50 microM glutamate for 15 min, at 22 degrees C, in the absence of Mg2+, about 80% of neurons were killed in about 24 hr. Exposure of neurons to such a pulse of glutamate, in the presence of various concentrations of amiloride, resulted in a dose-dependent protection from neurotoxicity (EC50 300 microM, complete protection 1 mM). In voltage-clamped cortical and cerebellar neurons of neonatal rats in primary culture, 100 microM amiloride diminished (by about 25%) glutamate- and/or NMDA-evoked cationic currents, recorded in the whole-cell mode. About 80% of the NMDA-(20 microM) stimulated current was inhibited by 700 microM amiloride. The inhibitory effect of amiloride was not voltage-dependent. In outside-out membrane patches, excised from granule cells and held at -50 mV, 100 microM amiloride changed the NMDA-elicited single channel activity into a fast flickering between the open and closed states. The noise analysis of the data revealed that, although resembling the Mg2(+)-induced flickering, the amiloride-induced channel block was more similar to the effects described for the action of local anaesthetics on the nicotinic cholinergic channel. The pharmacological relevance of this action of amiloride requires further characterization; the data point out the necessity of a cautious use of amiloride in studying neuronal function.

Amiloride↗
PubMed1995

Inhibition by folded isomers of L-2-(carboxycyclopropyl)glycine of glutamate uptake via the human glutamate transporter hGluT-1.

The effects of isomers of 2-(carboxycyclopropyl)glycine (CCG) on uptake of L-glutamate were investigated in COS-7 cells that expressed a cloned human glutamate transporter (hGluT-1). The (2S, 3S, 4R)-isomer (L-CCG-III) and the (2S, 3R, 4S)-isomer (L-CCG-IV) markedly inhibited glutamate uptake with a 50% inhibitory concentration of 290 nM and 1.1 microM, respectively. The (2S, 3S, 4S)-isomer (L-CCG-I) and the (2S, 3R, 4R)-isomer (L-CCG-II) did not inhibit glutamate uptake at concentrations of < or = 10 microM. Thus, hGluT-1 showed a markedly higher affinity for L-CCG-III and L-CCG-IV with a folded conformation of the glutamate skeleton, than for L-CCG-I or L-CCG-II with an extended conformation.

ATP-Binding Cassette Transporters↗
PubMed2005

Simultaneous detection of the release of glutamate and nitric oxide from adherently growing cells using an array of glutamate and nitric oxide selective electrodes.

The simultaneous detection of nitric oxide and glutamate using an array of individually addressable electrodes, in which the individual electrodes in the array were suitably modified with a highly sensitive nitric oxide sensing chemistry or a glutamate oxidase/redox hydrogel-based glutamate biosensor is presented. In a sequence of modification steps one of the electrodes was covered first with a positively charged Ni porphyrin entrapped into a negatively charged electrodeposition paint followed by the manual modification of the second working electrode by a bienzyme sensor architecture based on crosslinked redox hydrogels with entrapped peroxidase and glutamate oxidase. Adherently growing C6-glioma cells were grown on membrane inserts and placed in close distance to the modified sensor surfaces. The current responses recorded at each electrode after stimulation of glutamate and NO release by means of K+ and bradykinin clearly demonstrate the ability of the individual electrode in the array to detect the analyte towards which its sensitivity and selectivity was targeted without interference from the neighbouring electrode or other analytes present in the test mixture.

Animals↗
PubMed2006

Determination of the activities of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase in a microfluidic system.

A microfluidic system for the analysis of the activities of glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) was fabricated. The device consists of a glass chip with a micro-electrochemical L-glutamate sensor and a polydimethylsiloxane (PDMS) sheet with a Y-shaped micro-flow channel. A sample solution and a substrate solution for the enzymes were introduced from two injection ports at the end of the flow channel. When the flows were stopped, substrates in a solution mixed immediately with either of the enzymes by diffusion in a mixing channel. L-glutamate produced by the enzymatic reaction of GOT or GPT in the flow channel was detected by using the L-glutamate sensor. A distinct current increase was observed immediately after mixing, and the initial slope of the response curve varied in proportion to the activity of GOT or GPT. The relation between the slope of the response curve and the enzyme activity was linear between 7 and 228 U l-1 for GOT and 9 and 250 U l-1 for GPT. The quality of the response curve was improved with an increase in the channel height. The measurement based on the rate analysis in the micro-flow channel facilitated the reduction of the influence of interferents. The influence of the viscosity of the sample solution was also checked for the analysis of real samples. The determination of the enzyme activities was also conducted in a system with micropumps fabricated for a sample injection. Two solutions could be mixed in the mixing channel, and the activity of the enzymes could be measured as in the experiments using microsyringe pumps.

Alanine Transaminase↗
PubMed2006

Role of glutamate receptors in the ventromedial hypothalamus in the regulation of female rat sexual behaviors. II. Behavioral effects of selective glutamate receptor antagonists AP-5, CNQX, and DNQX.

Bilateral infusions of glutamate or its selective ionotrophic receptor agonists to the ventromedial hypothalamus (VMH) produce a rapid inhibition of both appetitive and consummatory sexual behavior in hormone-primed female rats. The present study examined whether infusion of selective ionotrophic glutamate receptor antagonists to the VMH can facilitate female sexual behavior in females treated with estradiol benzoate (EB) and progesterone (P), or EB alone. Ovariectomized, sexually experienced female rats were implanted bilaterally with guide cannulae aimed at the ventrolateral VMH. After recovery from surgery, females were primed either with EB+P or EB alone, and infused with saline, or one of two doses each of AP-5 (to target NMDA receptors), CNQX, or DNQX (to target AMPA/kainate receptors), immediately before tests with sexually vigorous male rats in bilevel chambers. In general, the drug infusions had a more powerful effect in females primed with EB alone compared to females primed with EB+P. AP-5 increased lordosis in females primed with EB alone. CNQX had a similar facilitative effect on lordosis, and also increased solicitations. DNQX increased solicitations in both hormone-priming conditions, increased lordosis quotients and magnitudes, and decreased pacing and defensive responses in the EB-alone condition. These results indicate that antagonism of glutamate receptors in the VMH resembles the effect of P, and that the addition of P to an EB baseline eliminates most of the effects of glutamate receptor antagonists. These data support the notion that glutamate receptors in the VMH contribute a strong inhibitory influence in the control of female sexual behavior.

2-Amino-5-phosphonovalerate↗
PubMed2002

Facilitation of glutamate release by ionotropic glutamate receptors in osteoblasts.

Constitutive expression of mRNA was seen for the vesicular glutamate transporter brain-specific Na(+)-dependent inorganic phosphate cotransporter (BNPI), but not differentiation-associated Na(+)-dependent inorganic phosphate cotransporter, in rat calvarial osteoblasts cultured for 7 and 21 days in vitro (DIV). Three different agonists for ionotropic glutamate receptors (iGluR) at 1mM, as well as 50mM KCl, significantly increased the release of endogenous L-glutamate from osteoblasts cultured for 7DIV when determined 5 min after the addition by using a high performance liquid chromatograph. The inhibitor of desensitization of DL-alpha-amino-3-hydroxy-5-methylisoxasole-4-propionate (AMPA) receptors cyclothiazide significantly potentiated and prolonged the release of endogenous L-glutamate evoked by AMPA in a dose-dependent manner. The release evoked by AMPA was significantly prevented by the addition of an AMPA receptor antagonist as well as by the removal of Ca(2+) ions. These results suggest that endogenous L-glutamate could be released from intracellular vesicular constituents associated with BNPI through activation of particular iGluR subtypes expressed in cultured rat calvarial osteoblasts.

Animals↗
PubMed1998

Spinal cord GLT-1 glutamate transporter and blood glutamic acid alterations in motor neuron degeneration (Mnd) mice.

This study characterizes for the first time neurochemical mechanisms in Mnd mice, initially described as a model of motor neuron disease and more recently proposed as a model for neuronal ceroid lipofuscinosis. A selective decrease (-30%) of [3H]glutamate uptake was found in spinal cord but not cortical synaptosomes of Mnd mice aged 28 weeks, when they show histopathological alterations, complete blindness and moderate neurological deficits. In spite of the widespread presence of stored material in neurons in many brain regions and spinal cord, the active transport of [3H]serotonin, [3H]dopamine and depolarization-induced [3H]serotonin release were not affected. Spinal EAAC1 glutamate transporter protein was significantly decreased in some but not all aged mice by 36% on average, possibly due to the loss of motor neurons. GLT-1 immunoreactivity was reduced by 34% in 28-week-old Mnd mice, while GLAST immunoreactivity was not affected. In Mnd mice aged 14 weeks, when there was no apparent alteration of motor function, the defect in the glial transporter protein GLT-1 was similar to that in 28-week-old mice (25%). Blood glutamic acid concentration was increased in Mnd mice aged 14-22 weeks. We suggest that the early decrease of GLT-1 protein might raise the extrasynaptic glutamic acid concentration, and contribute to the loss of motor neurons in affected mice, resulting in low [3H]glutamate uptake, low EAAC1 immunoreactivity and neurological deficits.

ATP-Binding Cassette Transporters↗
PubMed2001

In vivo microdialysis and immunohistochemical analyses of tendon tissue demonstrated high amounts of free glutamate and glutamate NMDAR1 receptors, but no signs of inflammation, in Jumper's knee.

This investigation describes, to our knowledge, the first experiment where the microdialysis technique was used to study certain metabolic events in human patellar tendons in combination with immunohistochemical analyses of tendon biopsies. In five patients (four men and one woman) with a long duration (range 12-36 months) of pain symptoms from Jumper's knee (localized tenderness in the patellar tendon verified as tendon changes with ultrasonography or MRI), and in five controls (four men and one woman) with normal patellar tendons, a standard microdialysis catheter was inserted into the patellar tendon under local anestesia. The local concentrations of glutamate (excitatory neurotransmitter) and prostaglandin E2 (PGE2) were registered under resting conditions. Samplings were done every 15 min during a 2 h period. In all individuals (patients and controls) biopsies were taken for immunohistochemical analyses. The results showed that it was possible to detect and measure the concentrations of glutamate and PGE2 in the patellar tendon with the use of microdialysis technique. There were significantly higher concentrations of free glutamate, but not PGE2, in tendons with tendinosis compared to normal tendons. In the biopsies, there were no inflammatory cell infiltrates, but, for the first time, it was shown that there was immunoreaction for the glutamate receptor NMDAR1 in association with nerve structures in human patellar tendons. These findings altogether indicate that glutamate might be involved in painful Jumper's knee, and further emphasizes that there is no chemical inflammation (normal PGE2 levels) in this chronic condition.

Adult↗
PubMedDate not supplied

Glutamate-like immunoreactivity in the cat superior colliculus and visual cortex: further evidence that glutamate is the neurotransmitter of the corticocollicular pathway.

Biochemical studies provide evidence that the pathway from visual cortex to the superior colliculus (SC) utilizes glutamate as a neurotransmitter. In the present study, we have used immunocytochemistry, visual cortex lesions, and retrograde tracing to show directly by anatomical methods that glutamate or a closely related analog is contained in corticocollicular neurons and terminals. A monoclonal antibody directed against gamma-L-glutamyl-L-glutamate (gamma glu glu) was used to localize glutamate-like immunoreactivity in both the superior colliculus (SC) and visual cortex (VC). Unilateral lesions of areas 17-18 were made in four cats to determine if gamma glu glu labeling was reduced in SC by this lesion. WGA-HRP was injected into the SC of 10 additional cats in order to determine if corticocollicular neurons were also labeled by the gamma glu glu antibody. A distinctive dense band of gamma glu glu immunoreactivity was found within the deep superficial gray and upper optic layers of SC where many corticotectal axons are known to terminate. Both fibers and cells were labeled within the band. Immunoreactivity was also found in cells and fibers throughout the deep layers of SC. Measures of total immunoreactivity (i.e. optical density) in the dense band were made in sections from the SC both ipsilateral to and contralateral to the lesions of areas 17-18. A consistent reduction in optical density was found in both the neuropil and in cells within the dense band of the SC ipsilateral to the lesion. A large percentage of all corticocollicular neurons that were retrogradely labeled by WGA-HRP also contained gamma glu glu. These results provide further evidence that the corticocollicular pathway in mammals is glutamatergic. The results also suggest that visual cortex ablation alters synthesis or storage of glutamate within postsynaptic SC neurons, presumably as a result of partial deafferentation.

Animals↗
PubMed2002

4-Substituted D-glutamic acid analogues: the first potent inhibitors of glutamate racemase (MurI) enzyme with antibacterial activity.

The first potent inhibitors of glutamate racemase (MurI) enzyme that show whole cell antibacterial activity are described. Optically pure 4-substituted D-glutamic acid analogues with (2R,4S) stereochemistry and bearing aryl-, heteroaryl-, cinnamyl-, or biaryl-methyl substituents represent a novel class of glutamate racemase inhibitors. Exploration of the D-Glu core led to the identification of lead compounds (-)-8 and 10. 2-Naphthylmethyl derivative 10 was found to be a potent competitive inhibitor of glutamate racemase activity (K(i) = 16 nM, circular dichroism assay; IC(50) = 0.1 microg/mL high-performance liquid chromatography (HPLC) assay). Thorough structure-activity relationship (SAR) studies led to benzothienyl derivatives such as 69 and 74 with increased potency (IC(50) = 0.036 and 0.01 microg/mL, respectively, HPLC assay). These compounds showed potent whole cell antibacterial activity against S. pneumoniae PN-R6, and good correlation with the enzyme assay. Compounds 69, 74 and biaryl derivative 52 showed efficacy in an in vivo murine thigh infection model against Streptococcus pneumoniae. Data described herein suggest that glutamate racemase may be a viable target for developing new antibacterial agents.

Amino Acid Isomerases↗
PubMed1975

Subcellular localization of gamma-aminobutyrate transaminase and glutamate dehydrogenase in adult rat brain. Evidence for at least two small glutamate compartments in brain.

The subcellular localizations of gamma-aminobutyrate transaminase (EC 2.6.1.19) and glutamate dehydrogenase (EC 1.4.1.2) in brain tissue of adult rats were compared with each other and with those of NAD+-isocitrate dehydrogenase (EC 1.1.41) and monoamine oxidase (EC 1.4.3.4; kynuramine as substrate). Crude mitochondrial fractions from brain tissue were centrifuged in continuous sucrose density gradients. gamma-Aminobutyrate transaminase and glutamate dehydrogenase were always found at a higher density than NAD+-isocitrate dehydrogenase and monoamine oxidase. When centrifuged for 1 h at 53 000gav., there was a slight difference between the distribution profiles of glutamate dehydrogenase and gamma-aminobutyrate transaminase. This difference was larger when the centrifugation time was only 15 min. It is concluded that there are subpopulations of brain mitochondria with differing proportions of gamma-aminobutyrate transaminase and glutamate dehydrogenase. The results are discussed in relation to evidence obtained with labelled precursors in vivo that there are at least two small glutamate compartments in adult brain.

4-Aminobutyrate Transaminase↗
PubMed2003

Nonlinear effects of glutamate and KCl on glutamate toxicity in cultured rat cerebellar neurons.

Nonlinear responses to toxin exposure have been observed in multiple cell types and organisms across a wide array of phyla. High dose toxin exposures inhibit or kill biological systems, while low dose exposures can stimulate survival mechanisms. We examined the effects of low (10(-3), 10(-5), 10(-7), and 10(-9) M) and ultra-low (10(-25) and 10(-61) M) KCl and glutamate pretreatment (72 h) against glutamate toxicity in rat cerebellar neurons. Ultra-low dilutions (10(-31), 10(-61), and 10(-401)) of an Arnica montana mother tincture were also investigated for their neuroprotective potentials. Viability was significantly enhanced in neurons pretreated with either 10(-3) M glutamate (10.6%) or 10(-9) M KCl (6.3%). None of the toxins evaluated displayed significant toxicity at the concentrations indicated. The protective effect of glutamate is likely mediated through activation of N-methyl-D-aspartate receptors, whereas low dose KCl might confer neuroprotection through enhanced alteration of Na+/K+ receptor dynamics. This is the first time high dose glutamate tolerance has been shown along with low dose KCl, and is consistent with previous reports demonstrating tolerance induced by low dose toxin exposure.

Analysis of Variance↗
PubMed2004

Monosodium glutamate and sweet taste: discrimination between the tastes of sweet stimuli and glutamate in rats.

Generalization of a conditioned taste aversion (CTA) is based on similarities in taste qualities shared by the aversive substance and another taste substance. CTA experiments with rats have found that an aversion to a variety of sweet stimuli will cross-generalize with monosodium glutamate (MSG) when amiloride, a sodium channel blocker, is added to all solutions to reduce the taste of sodium. These findings suggest that the glutamate anion elicits a sweet taste sensation in rats. CTA experiments, however, generally do not indicate whether two substances have different taste qualities. In this study, discrimination methods in which rats focused on perceptual differences were used to determine if they could distinguish between the tastes of MSG and four sweet substances. As expected, rats readily discriminated between two natural sugars (sucrose, glucose) and two artificial sweeteners (saccharin, SC45647). Rats also easily discriminated between MSG and glucose, saccharin and, to a lesser extent, SC45647 when the taste of the sodium ion of MSG was reduced by the addition of amiloride to all solutions, or the addition of amiloride to all solutions and NaCl to each sweet stimulus to match the concentration of Na+ in the MSG solutions. In contrast, reducing the cue function of the Na+ ion significantly decreased their ability to discriminate between sucrose and MSG. These results suggest that the sweet qualities of glutamate taste is not as dominate a component of glutamate taste as CTA experiments suggest and these qualities are most closely related to the taste qualities of sucrose. The findings of this study, in conjunction with other research, suggest that sweet and umami afferent signaling may converge through a taste receptor with a high affinity for glutamate and sucrose or a downstream transduction mechanism. These data also suggest that rats do not necessarily perceive the tastes of these sweet stimuli as similar and that these sweet stimuli are detected by multiple sweet receptors.

Animals↗