Journal articles: 'Excitatory amino acid'

1

SHINOZAKI, Haruhiko. "Excitatory amino acid receptors." Folia Pharmacologica Japonica 104, no. 3 (1994): 177–87. http://dx.doi.org/10.1254/fpj.104.177.

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2

Shinozaki, Haruhiko. "Excitatory amino acid receptors." Japanese Journal of Pharmacology 64 (1994): 35. http://dx.doi.org/10.1016/s0021-5198(19)49891-0.

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3

Gaviraghi, G. "Excitatory amino acid receptors." Pharmaceutica Acta Helvetiae 74, no. 2-3 (March 2000): 219–20. http://dx.doi.org/10.1016/s0031-6865(99)00052-7.

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4

Hicks, T. P., D. Lodge, H. McClennan, J. A. Hardy, and R. F. Cowburn. "Excitatory amino acid transmission." FEBS Letters 220, no. 2 (August 17, 1987): 395. http://dx.doi.org/10.1016/0014-5793(87)80857-8.

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5

Johnson, Rodney L., and James F. Koerner. "Excitatory amino acid neurotransmission." Journal of Medicinal Chemistry 31, no. 11 (November 1988): 2057–66. http://dx.doi.org/10.1021/jm00119a001.

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6

Ben-Ari, Y. "Excitatory amino acid receptors." Trends in Neurosciences 16, no. 7 (July 1993): 291. http://dx.doi.org/10.1016/0166-2236(93)90184-n.

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7

COLLINGRIDGE, G. L. "EXCITATORY AMINO ACID RECEPTORS." Behavioural Pharmacology 6, no. 5 (August 1995): 618. http://dx.doi.org/10.1097/00008877-199508000-00034.

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8

Attwell, David. "Excitatory amino acid antagonists." Trends in Pharmacological Sciences 12 (January 1991): 315–16. http://dx.doi.org/10.1016/0165-6147(91)90584-f.

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9

Johnson, Graham. "Excitatory amino acid related agents." Bioorganic & Medicinal Chemistry Letters 3, no. 1 (January 1993): 9–14. http://dx.doi.org/10.1016/s0960-894x(00)80082-7.

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10

Iversen, Leslie L., and Kennedy R. Lees. "6 Excitatory amino acid antagonists." Baillière's Clinical Anaesthesiology 10, no. 3 (September 1996): 481–96. http://dx.doi.org/10.1016/s0950-3501(96)80030-4.

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11

Smith, D. A. S., and N. Burton. "Excitatory amino acid receptor nomenclature." Trends in Neurosciences 9 (January 1986): 315. http://dx.doi.org/10.1016/0166-2236(86)90095-0.

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12

Rowley, Michael, and Paul D. Leeson. "Overview: Excitatory Amino Acid Antagonists." Current Opinion on Therapeutic Patents 2, no. 8 (August 1992): 1201–21. http://dx.doi.org/10.1517/13543776.2.8.1201.

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13

Chapman, Astrid G., and Brian S. Meldrum. "Excitatory amino acid antagonists and epilepsy." Biochemical Society Transactions 21, no. 1 (February 1, 1993): 106–10. http://dx.doi.org/10.1042/bst0210106.

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14

Lee, Victor, Jack Baldwin, and William Goundry. "Synthesis of Excitatory Amino Acid Analogues." Synlett 2006, no. 15 (September 2006): 2407–10. http://dx.doi.org/10.1055/s-2006-950399.

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15

Zamorano, Pedro L., Virendra B. Mahesh, Liesl De Sevilla, and Darrell W. Brann. "Excitatory Amino Acid Receptors and Puberty." Steroids 63, no. 5-6 (May 1998): 268–70. http://dx.doi.org/10.1016/s0039-128x(98)00033-6.

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16

Bruns, Robert F. "Nomenclature for excitatory amino acid receptors." Trends in Neurosciences 9 (January 1986): 62. http://dx.doi.org/10.1016/0166-2236(86)90023-8.

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17

Meyer, Ronald L. "Activity and excitatory amino acid receptors." Progress in Neuro-Psychopharmacology and Biological Psychiatry 17, no. 5 (September 1993): 681–90. http://dx.doi.org/10.1016/0278-5846(93)90052-t.

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18

Ulas, J., and C. W. Cotman. "Excitatory Amino Acid Receptors in Schizophrenia." Schizophrenia Bulletin 19, no. 1 (January 1, 1993): 105–17. http://dx.doi.org/10.1093/schbul/19.1.105.

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19

Meldrum, B. S. "Excitatory Amino Acid Transmitters in Epilepsy." Epilepsia 32, s2 (June 1991): S1—S3. http://dx.doi.org/10.1111/j.1528-1157.1991.tb05879.x.

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20

Garthwaite, J. "Excitatory amino acid receptors and channels." European Journal of Pharmacology 183, no. 1 (July 1990): 150. http://dx.doi.org/10.1016/0014-2999(90)91419-c.

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21

Nishikawa, Toru. "Schizophrenia and excitatory amino acid neurotransmission." Neuroscience Research Supplements 16 (January 1991): IV. http://dx.doi.org/10.1016/0921-8696(91)90603-k.

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22

Dingledine, Raymond, Chris J. McBain, and James O. McNamara. "Excitatory amino acid receptors in epilepsy." Trends in Pharmacological Sciences 11, no. 8 (August 1990): 334–38. http://dx.doi.org/10.1016/0165-6147(90)90238-4.

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23

Lodge, David, and Kenneth M. Johnson. "Noncompetitive excitatory amino acid receptor antagonists." Trends in Pharmacological Sciences 11, no. 2 (February 1990): 81–86. http://dx.doi.org/10.1016/0165-6147(90)90323-z.

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24

Matthews, James C., and Kevin J. Anderson. "Recent advances in amino acid transporters and excitatory amino acid receptors." Current Opinion in Clinical Nutrition and Metabolic Care 5, no. 1 (January 2002): 77–84. http://dx.doi.org/10.1097/00075197-200201000-00014.

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25

Nakase, Hiroyuki, Takaoki Tada, Takahiko Eguchi, Hidehiro Hirabayashi, Tetsuya Morimoto, and Toshisuke Sakaki. "Kindling Seizure Induction and Excitatory Amino Acid." Psychiatry and Clinical Neurosciences 46, no. 2 (June 1992): 357–60. http://dx.doi.org/10.1111/j.1440-1819.1992.tb00874.x.

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26

Chisamore, Brian, Mark Solc, and Kimberly Dow. "Excitatory amino acid regulation of astrocyte proteoglycans." Developmental Brain Research 97, no. 1 (November 1996): 22–28. http://dx.doi.org/10.1016/s0165-3806(96)00129-0.

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27

Girault, Jean-Antoine, Shelley Halpain, and Paul Greengard. "Excitatory amino acid antagonists and Parkinson's disease." Trends in Neurosciences 13, no. 8 (August 1990): 325–26. http://dx.doi.org/10.1016/0166-2236(90)90140-6.

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28

Ulshafer, Robert J., David M. Sherry, Ralph Dawson, and David R. Wallace. "Excitatory amino acid involvement in retinal degeneration." Brain Research 531, no. 1-2 (October 1990): 350–54. http://dx.doi.org/10.1016/0006-8993(90)90800-q.

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29

Buchanan, J. T., L. Brodin, N. Dale, and S. Grillner. "Reticulospinal neurones activate excitatory amino acid receptors." Brain Research 408, no. 1-2 (April 1987): 321–25. http://dx.doi.org/10.1016/0006-8993(87)90397-0.

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30

Gesemann, Matthias, Colette M. Maurer, and Stephan C. F. Neuhauss. "Excitatory amino acid transporters in the zebrafish." Brain Research Bulletin 83, no. 5 (October 2010): 202–6. http://dx.doi.org/10.1016/j.brainresbull.2010.04.018.

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31

MITCHELL, I. J. "STRIATAL EXCITATORY AMINO ACID TRANSMISSION AND PARKINSONISM." Behavioural Pharmacology 6, no. 5 (August 1995): 627. http://dx.doi.org/10.1097/00008877-199508000-00060.

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32

MACDERMOTT, A. "Transmitters and Receptors: Excitatory Amino Acid Transmission." Science 237, no. 4821 (September 18, 1987): 1517–18. http://dx.doi.org/10.1126/science.237.4821.1517-a.

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33

YONEDA, Yukio. "Receptive Mechanisms of Excitatory Amino Acid Signals." YAKUGAKU ZASSHI 113, no. 7 (1993): 469–88. http://dx.doi.org/10.1248/yakushi1947.113.7_469.

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34

Machtens, Jan-Philipp, Christine Lansche, Ariane Leinenweber, Petra Kilian, Birgit Begemann, Ulrich Zachariae, David Ewers, Bert L. de Groot, Rodolfo Briones, and Christoph Fahlke. "Anion Permeation through Excitatory Amino Acid Transporters." Biophysical Journal 106, no. 2 (January 2014): 149a. http://dx.doi.org/10.1016/j.bpj.2013.11.858.

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35

Glavin, Gary B., Carl Pinsky, and Ranjan Bose. "Mussel poisoning and excitatory amino acid receptors." Trends in Pharmacological Sciences 10, no. 1 (January 1989): 15–16. http://dx.doi.org/10.1016/0165-6147(89)90097-7.

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36

Collingridge, Graham L., and Wolf Singer. "Excitatory amino acid receptors and synaptic plasticity." Trends in Pharmacological Sciences 11, no. 7 (July 1990): 290–96. http://dx.doi.org/10.1016/0165-6147(90)90011-v.

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37

Meldrum, Brian, and John Garthwaite. "Excitatory amino acid neurotoxicity and neurodegenerative disease." Trends in Pharmacological Sciences 11, no. 9 (September 1990): 379–87. http://dx.doi.org/10.1016/0165-6147(90)90184-a.

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38

BARNES, J., and J. HENLEY. "Molecular characteristics of excitatory amino acid receptors." Progress in Neurobiology 39, no. 2 (August 1992): 113–33. http://dx.doi.org/10.1016/0301-0082(92)90007-2.

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39

Cain, Donald P. "Excitatory neurotransmitters in kindling: Excitatory amino acid, cholinergic, and opiate mechanisms." Neuroscience & Biobehavioral Reviews 13, no. 4 (December 1989): 269–76. http://dx.doi.org/10.1016/s0149-7634(89)80062-4.

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40

Curry, Kenneth. "Rigid analogues as probes of excitatory amino acid receptors." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 1076–83. http://dx.doi.org/10.1139/y91-159.

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The classes of coumpounds to be discussed are based on rigid analogues of glutamic and aspartic acids. The glutamate analogue 1-amino-1,3-cyclopentane dicarboxylic acid (1,3-ACPD) exists as two enantiomeric pairs of geometric isomers. The absolute configurations were assigned and the compounds were found to differentiate between the kainic acid (KA) and N-methyl-D-aspartic acid (NMDA) receptor subtypes when applied iontophoretically to hippocampal CA1 pyramidal neurones. The results indicate a high degree of specificity for the interaction of D-cis- 1,3-ACPD with the NMDA receptor, while the remaining three isomers of 1,3-ACPD were KA-like in their action. The results are augmented with binding studies and patch clamp analysis. The second class of compound is the closely related aspartate analogue 1-amino-1,2-cyclopentane dicarboxylic acid (1,2-ACPD). The geometric isomers have been examined and found to be somewhat less active than their 1,3-ACPD counterparts; however, the cis isomer does have antagonistic properties against quisqualate (QA) evoked excitation. The results indicate that while the three-dimensional arrangement of functional groups is important for the activation of receptor subtypes, other considerations must be made, including stereochemistry and receptor affinity for sterically hindered analogues of excitatory amino acids.Key words: excitatory amino acids, electropharmacology, receptor mapping, rigid analogues.

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41

Watkins, J. C. "Some chemical highlights in the development of excitatory amino acid pharmacology." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 1064–75. http://dx.doi.org/10.1139/y91-158.

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Important findings in the excitatory amino acid (EAA) field that have stemmed directly from work initiated in chemical laboratories are discussed from a historical point of view, showing how each has contributed to our present knowledge of EAA receptors. The groups of compounds discussed include simple analogues and derivatives of short-chain excitatory amino acids, longer-chain analogues, analogues containing ring structures essential to the acidic nature of the ω-terminal, and conformationally restricted agonists and antagonists. Recent interest has centred on antagonists for the N-methyl-D-aspartate (NMDA) and α-methyl-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptors typified by the long-chain ω-phosphono amino acids and the quinoxalinediones, respectively. Consideration of conformational aspects of both agonists and antagonists is currently providing considerable insight into the disposition of charged sites and general topological features in the various receptors, as well as the likely conformation adopted by L-glutamate in its physiological interaction with these receptors.Key words: excitatory amino acid receptors, historical development, structure–activity relations, NMDA receptors, AMPA receptors, kainate receptors.

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42

Ornstein, Paul, M. Brian Arnold, Nancy Allen, and Darryle Schoepp. "Synthesis and Characterization of Phosphonic Acid-Substituted Amino Acids as Excitatory Amino Acid Receptor Antagonists." Phosphorus, Sulfur, and Silicon and the Related Elements 109, no. 1 (1996): 309–12. http://dx.doi.org/10.1080/10426509608545152.

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43

Weiss, John H., and Dennis W. Choi. "Differential Vulnerability to Excitatory Amino Acid-Induced Toxicity and Selective Neuronal Loss in Neurodegenerative Diseases." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S3 (August 1991): 394–97. http://dx.doi.org/10.1017/s0317167100032522.

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ABSTRACT:Neurodegenerative diseases are characterized by selective degeneration of certain biochemically distinct subpopulations of central neurons. Studies of the intrinsic vulnerability of such neurons to injury by excitatory amino acids in vitro, as well as study of neurologic syndromes produced in animals or humans by ingestion of environmental excitatory amino acid neurotoxins may suggest a link between excitotoxicity, and the pathogenesis of certain neurodegenerative diseases.

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44

Stonik, Valentin A., and Inna V. Stonik. "Marine Excitatory Amino Acids: Structure, Properties, Biosynthesis and Recent Approaches to Their Syntheses." Molecules 25, no. 13 (July 3, 2020): 3049. http://dx.doi.org/10.3390/molecules25133049.

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This review considers the results of recent studies on marine excitatory amino acids, including kainic acid, domoic acid, dysiherbaine, and neodysiherbaine A, known as potent agonists of one of subtypes of glutamate receptors, the so-called kainate receptors. Novel information, particularly concerning biosynthesis, environmental roles, biological action, and syntheses of these marine metabolites, obtained mainly in last 10–15 years, is summarized. The goal of the review was not only to discuss recently obtained data, but also to provide a brief introduction to the field of marine excitatory amino acid research.

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45

Gordon, F. J. "Aortic baroreceptor reflexes are mediated by NMDA receptors in caudal ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 3 (March 1, 1987): R628—R633. http://dx.doi.org/10.1152/ajpregu.1987.252.3.r628.

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The purpose of this study was to identify central nervous system pathways and synaptic receptors that participate in baroreflex control of arterial pressure. Microinjections of excitatory amino acids into the caudal ventrolateral medulla (CVM) of anesthetized rats evoked depressor responses analogous to baroreceptor reflexes. Functional inactivation of CVM neurons produced by microinjection of the gamma-aminobutyric acid receptor agonist muscimol completely abolished baroreflex-mediated decreases in arterial pressure elicited by electrical stimulation of the aortic nerve and markedly reduced depressor responses produced by the excitatory amino acid L-glutamate. In contrast, selective blockade of N-methyl-D-aspartic acid (NMDA) receptors in the CVM abolished synaptically mediated depressor responses evoked by aortic nerve stimulation but not those elicited by L-glutamate, kainic acid, or quisqualic acid injected at the same site. These results indicate that the CVM contains an obligatory synapse in the central aortic baroreflex pathway; neural transmission of aortic baroreceptor information in the CVM is mediated by activation of NMDA receptors; and the neurotransmitter released at CVM synapses may be an excitatory amino acid.

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46

Mora, Francisco, and Alberto Porras. "Effects of amphetamine on the release of excitatory amino acid neurotransmitters in the basal ganglia of the conscious rat." Canadian Journal of Physiology and Pharmacology 71, no. 5-6 (May 1, 1993): 348–51. http://dx.doi.org/10.1139/y93-054.

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The effects of systemic injections of amphetamine sulfate on the release of aspartic acid, glutamic acid, and glutamine were studied using a push–pull perfusion system in the conscious rat. Amphetamine produced a dose-related increase of the extracellular levels of aspartic acid and glutamic acid. The mean time effect of amphetamine was 40 min, followed by a recovery to baseline levels. The mean percentage increase in amino acids released by the highest dose of amphetamine (5 mg/kg) was as follows: Asp, 334.6%; Glu, 224.5%; and Gln, 317.6%. All these effects were blocked by the dopamine D1–D2 receptor blocker haloperidol. It is suggested that dopamine, released by amphetamine, induces the release of amino acid neurotransmitters in the neostriatum. In addition, it is proposed that dopamine could mediate the neurotoxic effects produced by amphetamines through their secondary action on the release of excitatory amino acids.Key words: amphetamine, dopamine, excitatory amino acids, neostriatum, conscious rat.

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47

Huang, M. H., F. M. Smith, and J. A. Armour. "Amino acids modify activity of canine intrinsic cardiac neurons involved in cardiac regulation." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 4 (April 1, 1993): H1275—H1282. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1275.

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The effects of amino acids on intrinsic cardiac neuronal activity identified in 10 anesthetized dogs were investigated. Local injection of small volumes (1-10 microliters) of the excitatory amino acids, glutamate (100 mM) and aspartate (10 mM), and the inhibitory amino acids, gamma-aminobutyric acid (GABA; 10 mM) and glycine (10 mM), modified the activity of 39 of 50 identified neurons. Spontaneous activity of eight neurons was modified by both excitatory and inhibitory amino acids. Cardiodynamic responses accompanied neuronal activity modification in 15 instances. After acute decentralization, repeat doses of amino acids altered the activity of 21 neurons and elicited cardiovascular responses in 7 instances. Neuronal and cardiovascular responses were elicited after atropine administration. Neuronal but not cardiac responses were elicited after subsequent timolol administration. In other animals, GABA but not other amino acids elicited neuronal and cardiodynamic responses after hexamethonium administration in decentralized preparations, indicating that non-nicotinic synapses were involved in some GABA-induced responses. These results demonstrate that excitatory and inhibitory amino acids can modify intrinsic cardiac neuronal activity such that, as a consequence, cardiac variables can be modified.

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48

Pullan, L. M., J. W. Olney, M. T. Price, R. P. Compton, W. F. Hood, J. Michel, and J. B. Monahan. "Excitatory Amino Acid Receptor Potency and Subclass Specificity of Sulfur-Containing Amino Acids." Journal of Neurochemistry 49, no. 4 (October 1987): 1301–7. http://dx.doi.org/10.1111/j.1471-4159.1987.tb10024.x.

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49

West, M., and W. Huang. "Spinal cord excitatory amino acids and cardiovascular autonomic responses." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (September 1, 1994): H865—H873. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h865.

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The excitatory amino acid subtype receptor agonists, N-methyl-D-aspartate (NMDA) and (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, a non-NMDA agonist), produce specific dose-related heart rate and vasoconstrictor responses when given by injection into the upper thoracic or lumbar intrathecal space of the conscious rabbit. The responses are inhibited by prior intrathecal injection of the specific excitatory amino acid subtype receptor antagonist, 2-amino-5-phosphonovaleric acid (AP-5) or 6,7-dinitroquinoxaline-2,3-dione (DNQX), respectively. Baroreceptor heart rate reflex function is inhibited by AP-5 and by DNQX applied to the upper thoracic spinal cord. In contrast baroreflex vasoconstrictor function is blocked by AP-5 but not by DNQX given in the lumbar intrathecal space. The experiments support previous evidence that spinal excitatory amino acids are important as neurotransmitters at the level of the sympathetic preganglionic neuron and as such exert tonic and reflex control of autonomic cardiovascular function. It is concluded that 1) intrathecal activation of NMDA and non-NMDA subtype receptors has similar but independent effects on heart rate and on blood pressure and 2) NMDA receptors alone participate in mediation of baroreflex vasoconstrictor function, whereas both sets of receptors determine reflex sympathetic heart rate effects.

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50

Dunlop, John, and John Butera. "Ligands Targeting the Excitatory Amino Acid Transporters (EAATs)." Current Topics in Medicinal Chemistry 6, no. 17 (September 1, 2006): 1897–906. http://dx.doi.org/10.2174/156802606778249829.

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Journal articles on the topic 'Excitatory amino acid'

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