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Books on the topic 'D-aspartate'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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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

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

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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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

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11

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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12

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

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13

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

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14

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

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15

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

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16

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

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17

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

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18

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

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19

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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20

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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21

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

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22

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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23

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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24

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

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25

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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26

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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27

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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28

Keshav, Satish, and Palak Trivedi. Viral hepatitis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0212.

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Hepatitis means ‘inflammation of the liver’ and is manifest with symptoms that include malaise, anorexia, fever, flu-like symptoms, and pain in the right upper quadrant of the abdomen, with the pain being caused by swelling of the liver and its capsule. Elevations in circulating hepatic enzymes, particularly aspartate transaminase and alanine transaminase, are common, with jaundice occurring some time after the onset of other symptoms and signs. There are five viruses that primarily cause viral hepatitis: hepatitis A, B, C, D, and E viruses, abbreviated HAV, HBV, HCV, HDV, and HEV, respectively. These viruses are all hepatotrophic, in that the liver is the primary site of infection. HAV, HBV, and HEV are usually acute, self-limiting infections that may, nonetheless, cause morbidity and, in the case of HEV, fatality. However, HBV and, more so, HCV can cause chronic carriage of the virus over many years, as well as the development of chronic hepatitis. HDV is only pathogenic in conjunction with HBV. After recovery from acute infection with HAV, individuals have long-lasting immunity against further infection. The same holds true for the majority of individuals with acute HBV infection. There seems to be little natural immunity to HCV infection, and a significant proportion of cases result in chronic hepatitis. Immunity to HEV is not long-lasting, and repeated infections are possible. Many other viruses can cause hepatitis, of which cytomegalovirus, herpes simplex virus, Epstein–Barr virus, and flaviviruses such as dengue and yellow fever are the most important. The liver, however, is not their primary site of replication or cellular damage.

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29

(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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