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1

Raouf, Ramin K. Functional regulation of N-methyl-D-aspartate receptors by serine/threonine protein kinases. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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2

Bartlett, Mary Claire. Modulation of N-methyl-D-aspartate currents in cultured hippocampal neurones by protein kinase C. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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3

Malenfant, Sylvie A. The N-methyl-D-aspartate receptor system mediates spatial learning but not maternal experience effects. Ottawa: National Library of Canada, 1990.

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4

Konarski, Jakub Z. Molecular mechanism of protein kinase C enhancement of N-methyl-D-aspartate receptor calcium-dependent inactivation. Ottawa: National Library of Canada, 2002.

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5

Wrong, Andrew D. Bimodal modulation of N-methyl-D-aspartate-induced currents in rat CA1 hippocampal neurons by kainate application. Ottawa: National Library of Canada, 2002.

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6

Moussa, Raffy Cesario. The effect of seizure activity on tyrosine phosphorylation of the N-methyl-D-aspartate receptor in the hippocampus. Ottawa: National Library of Canada, 2002.

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7

Vij, Shilpa. Differential phosphorylation of the NR1 subunit of the N-methyl-D-aspartate receptor following hypoxia-ischemia in 7-and 21-day old rat brains. Ottawa: National Library of Canada, 2003.

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8

A, Cavalheiro Esper, Lehmann John 1952-, and Turski Lechoslaw, eds. Frontiers in excitatory amino acid research: Proceedings of an International Symposium "Excitatory Amino Acids '88," held in Manaus, Amazonas, Brazil, March 28-April 2, 1988. New York: Liss, 1988.

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9

Wells, Elizabeth M. Anti-N-Methyl-D-Aspartate Receptor Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0091.

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Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe but treatable recently identified form of immune-mediated encephalitis associated with antibodies in serum and cerebrospinal fluid (CSF) against the GluN1 subunit of the NMDAR. Research has rapidly expanded the understanding of disease mechanisms and how the condition manifests in different populations (e.g., pediatrics vs. adult, cancer vs. noncancer, male vs. female). Immunocytochemical, physiological, and molecular studies of the effects of human CSF on the rodent and murine brain in vitro and in vivo indicate a noncytotoxic antibody-mediated mechanism of disease pathogenesis. Finding positive antibodies prompts a search for occult neoplasm, most likely ovarian teratoma in young women; other age groups and male patients are less likely to have tumor but need to be screened. Fifty percent of patients respond to first line steroids, IVIG, plasma exchange or a combination, and many others improve with addition of rituximab or cyclophosphamide. Cured patients may have cognitive or motor sequelae, and refractory disease and death may occur despite treatment. Knowledge about etiology and biomarkers of refractory disease are lacking. Additional work is needed to further elucidate the origin of the immune-mediated response, to determine optimal clinical management and develop effective therapies for refractory patients.
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10

Biology of the NMDA receptor. Boca Raton, Fla: Taylor & Francis, 2008.

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11

Biology of the NMDA Receptor (Frontiers in Neuroscience). CRC, 2008.

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12

Roth, Jane. Interaction of dextrorotatory opioids with the N-methyl-D-aspartate receptor. 1995.

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13

P, Kozikowski Alan, and Barrionuevo German, eds. Neurobiology of the NMDA receptor: From chemistry to the clinic. New York, N.Y: VCH, 1991.

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14

1962-, Li Min, ed. NMDA receptor protocols. Totowa, N.J: Humana Press, 1999.

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15

Kozikowski, Alan. Neurobiology of the Nmda Receptor: From Chemistry to the Clinic. Vch Pub, 1991.

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16

L, Collingridge G., and Watkins J. C, eds. The NMDA receptor. 2nd ed. Oxford: Oxford University Press, 1994.

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17

B, De Souza Errol, Clouet Doris H, London Edythe D, and National Institute on Drug Abuse., eds. Sigma, PCP, and NMDA receptors. Rockville, MD (5600 Fishers Lane, Rockville 20857): U.S. Dept. of Health and Human Services, Public Health Service, Substance Abuse and Mental Health Services Administration, National Institute on Drug Abuse, 1993.

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18

Kotecha, Suhas. G-protein coupled receptor modulation of N-Methyl-D-aspartate channel activity. 2001.

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19

Macdonald, Daniel Scott. Modulation of N-methyl-D-aspartate receptors by pituitary adenylate cyclase activating peptide. 2006.

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20

Cheung, Herman Ho-Man. Phosphorylation of the N-methyl-D-Aspartate receptor in control and ischemic rat brain. 2002.

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21

Mozzarelli, Andrea, and Robert S. Phillips, eds. Enzymes Regulating the Homeostasis of Agonists and Antagonists of the N-Methyl D-Aspartate Receptors. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-062-2.

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22

Xu, Jindong. The role of C-terminial SRC kinase (Csk) in the regulation of N-methyl-D-aspartate receptors. 2006.

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23

Brooks, William James *. The role of the N-methyl-D-aspartate receptor in synaptic structural plasticity: possible implications for learning. 1991.

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24

Sattler, Rita. Cellular and molecular mechanisms of N-methyl-D-aspartate receptor mediated calcium-dependent neurotoxicity in cortical cell cultures. 1999.

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25

B, De Souza Errol, Clouet Doris H, London Edythe D, and National Institute on Drug Abuse., eds. Sigma, PCP, and NMDA receptors. Rockville, MD (5600 Fishers Lane, Rockville 20857): U.S. Dept. of Health and Human Services, Public Health Service, Substance Abuse and Mental Health Services Administration, National Institute on Drug Abuse, 1993.

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26

Dalip J.S. Sirinathsinghji (Editor) and Ray G. Hill (Editor), eds. NMDA antagonists as potential analgesic drugs (Progress in Inflammation Research). Birkhäuser Basel, 2002.

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27

Kitay, Brandon M., and Rajesh R. Tampi. Memantine in Patients with Moderate to Severe Alzheimer’s Disease Already Receiving Donepezil. Edited by Ish P. Bhalla, Rajesh R. Tampi, Vinod H. Srihari, and Michael E. Hochman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190625085.003.0018.

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This chapter provides a summary of a landmark study on the pharmacological management of cognitive disorders. In patients with moderate to severe Alzheimer disease treated with a cholinesterase inhibitor (donepezil), is the addition of a N-methyl-D-aspartate receptor inhibitor (memantine) a safe and efficacious augmentation strategy? Starting with that question, it describes the basics of the study, including funding, study location, who was studied, how many patients, study design, study intervention, follow-up, endpoints, results, and criticism and limitations. The chapter briefly reviews other relevant studies and controversy within the field, concluding with a discussion of implications, and an exemplary clinical case applying the study evidence.
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28

International review of neurobiology. Vol. 56. San Diego, Calif: Academic, 2003.

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29

C, Watkins J., and Collingridge G. L, eds. The NMDA receptor. Oxford: IRL Press at Oxford University Press, 1989.

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30

The NMDA Receptor. Oxford University Press, USA, 1990.

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31

C, Watkins J., Collingridge G. L, and British Pharmacological Society, eds. The NMDA receptor. Oxford: IRL Press at Oxford University Press, 1989.

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32

Frontiers in excitatory amino acid research: Proceedings of an International Symposium "Excitatory Amino Acids '88," held in Manaus, Amazonas, Brazil, ... 2, 1988 (Neurology and neurobiology). Liss, 1988.

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33

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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34

Hubbard, Claire Margaret. On the mechanisms of aluminum ion-induced neurotoxicity: The effects of aluminum species on G-protein-mediated processes and on drug interactions with the N-methyl-D-aspartate modulated ionophore. 1989.

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35

Jean-Marc, Kamenka, Domino Edward F. 1924-, and French-U.S. Seminar CNRS/NSF on Multiple Sigma and PCP Receptor Ligands: Mechanisms for Neuromodulation and Protection? (3rd : 1991 : La Grande Motte, France), eds. Multiple sigma and PCP receptor ligands: Mechanisms for neuromodulation and neuroprotection? Ann Arbor, Mich: NPP Books, 1992.

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36

Kamenka, J. M. Multiple Sigma and Phencyclidine Receptor Ligands: Mechanisms for Neuromodulation and Protection. Npp Books, 1992.

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37

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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38

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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