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Books on the topic 'NMDA receptors and metabotropic glutamate receptors'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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1

Baskys, Andrius. Metabotropic glutamate receptors. Austin: R.G. Landes Co., 1994.

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2

Conn, P. Jeffrey, and Jitendra Patel, eds. The Metabotropic Glutamate Receptors. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2298-7.

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3

Blythe, Louise Jane. Analysis of presynaptic metabotropic glutamate and adenosine A1 receptors. Ottawa: National Library of Canada, 1998.

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4

Hornby, Geoffrey. Radioligand binding analyses of the group III metabotropic glutamate receptors. Ottawa: National Library of Canada, 1999.

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5

International Meeting on Metabotropic Glutamate Receptors (2nd 1996 Taormina, Italy). Metabotropic glutamate receptors and brain function: Proceedings of the 2nd International Meeting on Metabotropic Glutamate Receptors held in Taormina, Italy, in September 1996. Edited by Moroni F, Nicoletti F, and Pellegrini-Giampietro D. E. London: Portland, 1998.

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6

Bruton, Rachel Kathlyn. An immunological and biochemical investigation of some cental metabotropic glutamate receptors (mGluRs). Birmingham: University of Birmingham, 1996.

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7

Naples, Mark. Determinants of high affinity ligand binding to the group III metabotropic glutamate receptors. Ottawa: National Library of Canada, 2001.

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8

Patel, Jitendra, and P. Jeffrey Conn. The Metabotropic Glutamate Receptors. Humana, 2010.

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9

The Metabotropic Glutamate Receptors. Humana Press, 2012.

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10

Jeffrey, Conn P., and Patel Jitendra, eds. The Metabotropic glutamate receptors. Totowa, N.J: Humana Press, 1994.

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11

Palazzo, Enza, Volker Neugebauer, and Sabatino Maione, eds. Metabotropic Glutamate Receptors and Neurological/Psychiatric Disorders. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-862-2.

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12

Rosemond, Erica Kim. Molecular pharmacology of the metabotropic glutamate receptors. 2005.

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13

O'Keeffe, Jordan. Metabotropic Glutamate Receptors: Classification, Structure and Roles in Disease. Nova Science Publishers, Incorporated, 2018.

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14

(Editor), F. Moroni, D. E. Pellegrini-Giampietro (Editor), and F. Nicoletti (Editor), eds. Metabotropic Glutamate Receptors and Brain Function (Portland Press Proceedings,). Ashgate Publishing, 1998.

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15

Noeske, Tobias. Ligand Binding in the Transmembrane Region of Metabotropic Glutamate Receptors. VDM Verlag Dr. Mueller e.K., 2007.

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16

Olive, M. Foster. Metabotropic Glutamate Receptors: Molecular Mechanisms, Role in Neurological Disorders and Pharmacological Effects. Nova Science Publishers, Incorporated, 2014.

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17

Steenland, Hendrick William. Respiratory activation of the genioglossus muscle involves both non-NMDA and NMDA glutamate receptors at the hypoglossal motor nucleus in-vivo. 2005.

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18

Koo, Joseph Chun Pong. Exploration of the essential requirements for the proteomic analysis of the metabotropic glutamate receptors by mass spectrometry. 2005.

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19

Koo, Joseph Chun Pong. Exploration of the essential requirements for the proteomic analysis of the metabotropic glutamate receptors by mass spectrometry. 2005.

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20

Nutt, David J., and Liam J. Nestor. The glutamate system and addiction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198797746.003.0009.

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Glutamate is the primary excitatory neurotransmitter in the brain. Glutamate is involved in synaptic plasticity, particularly within dopamine systems of the brain that are involved in reward. Glutamate-dependent plasticity is involved in the development of substance addiction through its actions at NMDA receptors during long-term potentiation (LTP) related learning and memory processes. This plasticity within brain circuitry involved in learning and memory is sustained during substance abstinence and may provide a neural substrate for a vulnerability to addiction relapse. Medications that possess the efficacy to reduce glutamate tone in certain brain circuits may reduce craving, and ultimately, relapse in substance dependence. Further research is required, however, to show that the modulation of glutamate transmission in the brain confers clinical benefits in substance addiction.
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21

Mason, Peggy. Receiving the Synaptic Message. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0013.

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Ionotropic and metabotropic receptors differ in their speed of action, the variety of effects produced after ligand-binding, and in the number of types present in the nervous system. The participation of two ionotropic glutamate receptors in synaptic plasticity is thought to be the cellular basis of learning. The actions of acetylcholine on nicotinic acetylcholine receptors present at the neuromuscular junction are described. The pharmacological profile of the GABAA receptor, central to most neural functions, is introduced. The properties of metabotropic receptors that are coupled to G proteins, termed G protein-coupled receptors (GPCRs), are detailed. Three canonical second-messenger systems through which GPCRs act are briefly described. An introduction to clinical pharmacology focused on how drugs acting on muscarinic and adrenergic receptors produce peripheral and central psychotropic effects is provided. Finally, the role of connexins and gap junctions in myelination and hearing is introduced.
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22

Black, Sheila. The original description of central sensitization. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0040.

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The landmark study discussed in this chapter is ‘The contribution of excitatory amino acids to central sensitization and persistent nociception after formalin-induced tissue injury’, published by Coderre and Melzack in 1992. Previous studies in this field implicate a contribution of excitatory amino acids (EAAs), specifically l-glutamate and l-aspartate, to injury-induced sensitization of nociceptive responses in the dorsal horn of the spinal cord. Repetitive stimulation of primary afferent fibres demonstrated that l-glutamate and NMDA can produce ‘wind-up’ of neuronal dorsal horn activity, and this is blocked by application of NMDA antagonists. This study uses the formalin test as a behavioural model to investigate the mechanisms underlying central sensitization and the role of EAAs, NMDA, their receptors, and their antagonists in this process.
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23

Ren, Ke, and Ronald Dubner. The first crystal structure of an ionotropic glutamate receptor ligand-binding core. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0032.

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The known functional ionotropic glutamate receptors (iGluRs) are composed of three major subtypes: AMPA, NMDA, and kainate. In 1998, in the landmark paper discussed in this chapter, Armstrong et al. provided the first crystal structure of an iGluR-subunit ligand-binding core, the S1S2 region of the rat GluA2 ‘flop’ isoform. They solved its structure with X-ray crystallography from selenomethonine crystals. They also identified residues involved in kainate binding, analysed allosteric sites that regulate affinity and specificity of the agonist, and mapped potential subunit–subunit interaction sites. They also proposed that binding of different agonists may result in variable degrees of domain closure. This work has profound impact on the field and it has been importantly cited. Subsequently, numerous high-resolution crystal structures of ligand-binding domains of iGluRs in complex with ligands, both agonists and antagonists, have been solved.
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24

Henter, Ioline D., and Rodrigo Machado-Vieira. Novel therapeutic targets for bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0030.

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The long-term course of bipolar disorder (BD) comprises recurrent depressive episodes and persistent residual symptoms for which standard therapeutic options are scarce and often ineffective. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors have consistently been implicated in the pathophysiology of mood disorders and in the development of novel therapeutics for these disorders. Since the rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000, other NMDA receptor antagonists have been studied in major depressive disorder (MDD) and BD. This chapter reviews the clinical evidence supporting the use of novel glutamate receptor modulators for treating BD—particularly bipolar depression. We also discuss other promising, non-glutamatergic targets for potential rapid antidepressant effects in mood disorders, including the cholinergic system, the melatonergic system, the glucocorticoid system, the arachidonic acid (AA) cascade, and oxidative stress and bioenergetics.
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