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Query: CAS:6893-26-1 (glutamate)
 73,096 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurons isolated from the medial subnuclei of nucleus tractus solitarius in adult guinea pigs were studied for responses to the excitatory amino acid glutamate and its analogues using the whole cell tight-seal voltage clamp technique. In 80% of the cells studied (n = 60) 100 microM glutamate produced inward currents at negative voltages. To further characterize the glutamate response, the agonists for three glutamate receptor subtypes, N-methyl-D-aspartate (NMDA), kainate, and quisqualate, were examined for their effects on membrane conductance. NMDA (25-250 microM) activated currents in 85% of the neurons tested (n = 30). NMDA currents were generally very small in amplitude. Of the neurons tested, 84% responded to kainate (10-30 microM, n = 19) and only 50% to quisqualate (25-50 microM, n = 26). The conductance activated by NMDA was outwardly rectifying. The conductance activated by kainate was voltage independent, while that activated by quisqualate showed varying degrees of outward rectification. Responses to NMDA were specifically antagonized by DL-2-amino-5-phosphonovaleric acid (AP-5, 50-100 microM). Kainate responses were blocked by kynurenate at concentrations (0.5-1.5 mM) ineffective on quisqualate-induced current. Glutamic acid diethyl ester (GDEE, 2-15 mM) was effective in reducing quisqualate responses at concentrations that had no effect on kainate responses. This characterization of the glutamate receptor subtypes and effective antagonists provides a basis for future determination of the specific receptor of glutamate responsible for mediation of the excitatory postsynaptic potentials produced by activation of the baroreceptor input.
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PMID:Excitatory amino acid receptors of guinea pig medial nucleus tractus solitarius neurons. 197 75

There is only limited information of the neurotransmitters in central respiratory control. L-glutamic acid has been proposed as the primary neurotransmitter in the nucleus of the tractus solitarius (NTS) in cats. To test whether there is a respiratory effect of glutamic acid in the respiratory center or not, we microinjected L-glutamic acid (1 M, 0.1 microliter) via 1 microliter Hamilton microsyringe into the ventrolateral nucleus of NTS, namely dorsal respiratory group (DRG) over two-second intervals with continuous monitoring of phrenic nerve activity (PNA), frequency (f), end tidal CO2, blood pressure and heart rate. Glutamate induced various respiratory changes including: increase in PNA and f decrease in PNA and f [corrected] increase in PNA but decrease in f and decrease in PNA but increase in f. In addition to regular changes of PNA or f elicited by glutamate microinjection were found. Other patterns of irregular rhythmic changes such as absence of PNA, continuous phrenic nerve discharge and irregular phrenic nerve discharge with reflex apnea, apneusis and irregular respiration respectively were also observed. Glutamic acid appears to significantly modulate respiratory drive in DRG. We suggested that L-glutamic acid may be a neurotransmitter in the respiratory center and be involved in central respiratory control.
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PMID:The different changes of phrenic nerve activity and frequency elicited by microinjection of L-glutamic acid into ventrolateral nucleus of the tractus solitarius in cats. 197 37

Glutamic acid and excitatory amino acids specific for the glutamate receptor subtypes were microinjected into the A10 region of the rat. Glutamate produced an increase in motor behavior that was antagonized by pretreatment with the dopamine D2 receptor antagonist, haloperidol. This motor stimulant effect was produced by kainate, but not by N-methyl-D-aspartate (NMDA) or quisqualic acid. By using in vivo dialysis it was found that dopamine release in the nucleus accumbens and locomotor activity were enhanced by glutamate injection into the A10 region. Whereas glutamate was found to increase the postmortem concentration of dopamine metabolites in the medial prefrontal cortex, nucleus accumbens and A10 region, NMDA selectively increased dopamine metabolism in the prefrontal cortex, and kainate produced increases in the nucleus accumbens and A10 region. When glutamate and the NMDA receptor antagonist, 3-[(+/-)-2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP) were coadministered, CPP selectively abolished the effect of glutamate on medial prefrontal cortical dopamine metabolites. A physiological role for the NMDA receptor modulation of A10 dopamine neurons was shown by intra-A10 pretreatment with CPP antagonism of mild footshock-induced increase in dopamine metabolites in the prefrontal cortex. These data argue that glutamate is a regulatory transmitter of A10 dopamine neurons, and that the NMDA receptor subtype modulates neurons projecting to the prefrontal cortex whereas the kainate subtype modulates mesoaccumbens neurons.
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PMID:Regulation of the mesocorticolimbic dopamine system by glutamic acid receptor subtypes. 255 79

The excitatory amino acids L-glutamate and N-methyl-D-aspartate (NMDA) produced contractions of the myenteric plexus-longitudinal muscle preparation of the guinea pig ileum over the concentration range of 3 X 10(-6) to 10(-3) M. The contractile response to L-glutamate and NMDA, but not carbamyl choline, was blocked noncompetitively by 0.6 mM Mg++. In the absence of Mg++, concentration-dependent increases in contractile force also were produced by, in order of potency, L-aspartate, L-homocysteate and D-glutamate, but not by quisqualate, kainate or quinolinate. L-Glutamate was competitively antagonized by the selective NMDA receptor antagonists D-2-amino-5-phosphonovalerate and 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (3 X 10(-6)-3 X 10(-5) M), as well as by the nonselective excitatory amino acid antagonist gamma-D-glutamylglycine (3 X 10(-4) M). Glutamic acid diethyl ester (3 X 10(-4) M) noncompetitively antagonized L-glutamate. L-Glutamate was not blocked by gamma-D-glutamylaminomethyl sulphonate (3 X 10(-4) M), an antagonist which preferentially antagonizes kainate and quisqualate. In addition, the phencyclidine-like drugs etoxadrol (10(-7)-10(-5) M), dextromethorphan (10(-6)-10(-5) M) and 5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imine (10(-9)-10(-7) M) noncompetitively antagonized L-glutamate. The (+) isomer of 5-methyl-10, 11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imine was approximately 10-fold more potent than the (-) isomer in antagonizing L-glutamate. The present results demonstrate that receptors for the excitatory amino acid L-glutamate are present in the guinea pig myenteric plexus and are of the NMDA subtype.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glutamate receptors of the N-methyl-D-aspartate subtype in the myenteric plexus of the guinea pig ileum. 257 91

Only limited information relating neurotransmitters to central regulation of the respiratory system exists. L-glutamic acid has been proposed as the primary neurotransmitter in the nucleus of the tractus solitarius (NTS) of cats. To test whether or not glutamic acid has an effect on the respiratory center, we microinjected L-glutamic acid (1 M, 0.1 microliter) via a 1 microliter Hamilton microsyringe into the ventrolateral area of the NTS dorsal respiratory groups (DRG) of unanesthetized, decerebrated cats at two-second intervals with continuous monitoring of tidal volume (VT), respiratory rate (f), end tidal CO2, blood pressure and heart rate. The results showed that glutamate induced the following respiratory changes: VT and f increased; VT and f decreased; and VT decreased but f increased. In addition to VT or f changes elicited by glutamate microinjection, changes in other rhythmic patterns such as apnea, apneusis and irregular respiration were observed. Glutamic acid appears to play a significant role in the modulation of the respiratory drive in the DRG. We, therefore, suggest that the excitatory amino acid L-glutamic acid may be involved in central respiratory control.
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PMID:Different respiratory patterns elicited by microinjection of L-glutamic acid into the ventrolateral nucleus of the tractus solitarius in cats. 257 3

Glutamic acid di-tert butyl ester (GTBE) was found to have a pronounced convulsant effect in mice and rats, producing recurrent clonic convulsions combined with postural and respiratory disturbances in a dosage of 0.5 mmol/kg (148 mg/kg). Tert-butyl ester derivatives of aspartic acid and alanine, and glutamic acid gamma-benzyl ester did not produce seizures. Various other glutamate esters, such as glutamic acid diethyl ester and glutamic acid dimethyl ester, have previously been found to have anticonvulsant effects, and also do not induce seizures. It is suggested that glutamic acid di-tert butyl ester may have specific pharmacological properties which differ from those of other known convulsant drugs.
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PMID:Convulsant properties of L-glutamic acid di-tert butyl ester. 286 66

The effect of intravenous glutamic acid infusion (3 mg/kg/min) was studied during myocardial ischemia and reperfusion in anesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Glutamic acid reduced the ischemic contractile depression 2 min after a 60%-reduction of the coronary blood flow. The left ventricular systolic pressure was decreased by 9% versus 22%, dP/dt by 16% versus 29%, left ventricular systolic pressure heart rate product by 16% versus 31%. Reperfusion with glutamic acid improved the recovery of cardiac performance without any increase in myocardial oxygen consumption. Glutamic acid infusion resulted in a 2-fold augmentation of glutamate uptake by the ischemic myocardium. It led to cessation of ammonia release by the heart due to activation of glutamine synthesis, enhancement of alanine formation coupled with pyruvate utilization and did not change lactate production. The mechanisms of the protective action of glutamic acid are discussed.
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PMID:[Correction of contractile function and metabolism in canine ischemic myocardium due to exogenous glutamic acid]. 286 92

The effect of intravenous infusion of glutamic acid on cardiac contractile function during short-term ischemia and subsequent reperfusion was studied in anaesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Infusion of glutamic acid at 3 mg/kg/min resulted in less depression of cardiac function when given after a 2 min period of 60% coronary blood flow reduction: left ventricular systolic pressure decreased by 9% vs. 22%, dP/dt decreased by 16% vs. 29%, the double product (left ventricular systolic pressure by heart rate) was reduced by 16% vs. 31%. When reperfusion was carried out during glutamic acid infusion there was a significantly enhanced recovery in cardiac function. The augmentation of cardiac performance in ischemia and reperfusion caused by glutamic acid was not accompanied by changes in myocardial oxygen consumption. Glutamic acid uptake by the ischemic myocardium increased 2-fold during infusion. This led to cessation of ammonia release from the heart due to stimulation of glutamine synthesis, and an enhancement of alanine formation coupled with pyruvate uptake but it did not effect lactate production. However, glutamic acid infusion did not influence cardiac performance and metabolism under conditions of normal coronary flow. The results suggest that elevation of glutamate arterial concentration exerts a beneficial effect on ischemic heart. The mechanisms of the protective action are discussed.
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PMID:Function and metabolism of dog heart in ischemia and in subsequent reperfusion: effect of exogenous glutamic acid. 286 19

Intravenous infusion of L-glutamic acid results in the augmentation of the cardiac output and an improvement of the circulation in patients with postoperative cardiac failure. This effect is not accompanied by increased myocardial oxygen demand. Arterial plasma glutamate level rises 10-fold and arterial-coronary sinus plasma glutamate difference increases fivefold during intravenous L-glutamic acid infusion. This leads to cessation of ammonia release from the myocardium, probably due to augmentation of glutamine synthesis and to an increase in alanine formation coupled with a change from lactate release to lactate uptake by the myocardium. The data obtained suggest that the beneficial effect of L-glutamic acid on depressed cardiac function in postoperative patients is related to changes in myocardial metabolism. Glutamic acid may be useful in treatment of circulatory and metabolic disturbances in cardiac failure.
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PMID:Cardiac metabolism and performance during L-glutamic acid infusion in postoperative cardiac failure. 286 48

Bath application of glutamate at two concentration ranges, 10(-6)-10(-8) and 1-3 X 10(-3) M, effectively increased acetylcholinesterase activity in cerebellar slices obtained from 8-day-old rats. No such effect was seen in cerebellar slices of 7-week-old rats or cerebral slices of either 7-week or 8-day-old rats. Glutamic acid diethyl ester blocked the glutamate effect at both of these concentration ranges, suggesting that quisqualate-sensitive glutamate receptors are involved in regulation of acetylcholinesterase activity in early postnatal cerebellum. Since bath application of cyclic GMP at 10(-7)-10(-9) M increased the acetylcholinesterase activity in cerebellar slices of 8-day-old rats, it is possible that glutamate-dependent regulation of acetylcholinesterase activity is mediated by cyclic GMP. The observation that adenosine deaminase blocked the effect of glutamate completely at 10(-6)-10(-8) M and partially at 1-5 X 10(-3) M further suggests that release of adenosine is a link from enhanced cyclic GMP activity to activation of acetylcholinesterase.
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PMID:Glutamate-elicited stimulation of acetylcholinesterase activity in cerebellar slices from newborn rats. 287 25


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