Relevant bibliographies by topics / Methyl aspartate

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Methyl aspartate'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Methyl aspartate"

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Deng, Meichun, Shao-Rui Chen, Hong Chen, and Hui-Lin Pan. "α2δ-1–Bound N-Methyl-d-aspartate Receptors Mediate Morphine-induced Hyperalgesia and Analgesic Tolerance by Potentiating Glutamatergic Input in Rodents." Anesthesiology 130, no. 5 (May 1, 2019): 804–19. http://dx.doi.org/10.1097/aln.0000000000002648.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Chronic use of μ-opioid receptor agonists paradoxically causes both hyperalgesia and the loss of analgesic efficacy. Opioid treatment increases presynaptic N-methyl-d-aspartate receptor activity to potentiate nociceptive input to spinal dorsal horn neurons. However, the mechanism responsible for this opioid-induced activation of presynaptic N-methyl-d-aspartate receptors remains unclear. α2δ-1, formerly known as a calcium channel subunit, interacts with N-methyl-d-aspartate receptors and is primarily expressed at presynaptic terminals. This study tested the hypothesis that α2δ-1–bound N-methyl-d-aspartate receptors contribute to presynaptic N-methyl-d-aspartate receptor hyperactivity associated with opioid-induced hyperalgesia and analgesic tolerance. Methods Rats (5 mg/kg) and wild-type and α2δ-1–knockout mice (10 mg/kg) were treated intraperitoneally with morphine twice/day for 8 consecutive days, and nociceptive thresholds were examined. Presynaptic N-methyl-d-aspartate receptor activity was recorded in spinal cord slices. Coimmunoprecipitation was performed to examine protein–protein interactions. Results Chronic morphine treatment in rats increased α2δ-1 protein amounts in the dorsal root ganglion and spinal cord. Chronic morphine exposure also increased the physical interaction between α2δ-1 and N-methyl-d-aspartate receptors by 1.5 ± 0.3 fold (means ± SD, P = 0.009, n = 6) and the prevalence of α2δ-1–bound N-methyl-d-aspartate receptors at spinal cord synapses. Inhibiting α2δ-1 with gabapentin or genetic knockout of α2δ-1 abolished the increase in presynaptic N-methyl-d-aspartate receptor activity in the spinal dorsal horn induced by morphine treatment. Furthermore, uncoupling the α2δ-1–N-methyl-d-aspartate receptor interaction with an α2δ-1 C terminus–interfering peptide fully reversed morphine-induced tonic activation of N-methyl-d-aspartate receptors at the central terminal of primary afferents. Finally, intraperitoneal injection of gabapentin or intrathecal injection of an α2δ-1 C terminus–interfering peptide or α2δ-1 genetic knockout abolished the mechanical and thermal hyperalgesia induced by chronic morphine exposure and largely preserved morphine’s analgesic effect during 8 days of morphine treatment. Conclusions α2δ-1–Bound N-methyl-d-aspartate receptors contribute to opioid-induced hyperalgesia and tolerance by augmenting presynaptic N-methyl-d-aspartate receptor expression and activity at the spinal cord level.
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Hsu, Chin, Jau-Nan Lee, Mei-Ling Ho, Bi-Hwa Cheng, Pi-Hseuh Shirley Li, and John Yuh-Lin Yu. "The facilitatory effect of N-methyl-D-aspartate on sexual receptivity in female rats through GnRH release." Acta Endocrinologica 128, no. 4 (April 1993): 385–88. http://dx.doi.org/10.1530/acta.0.1280385.

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The purpose of this study was to examine whether N-methyl-D-aspartate affects the sexual receptivity of female rats. Monosodium L-glutamate was used as a neurotoxin to induce hypogonadal status. Matured normal and monosodium L-glutamate-treated rats were ovariectomized and implanted subcutaneously with estradiol capsules. One week later, lordosis responsiveness was observed before and 10 min after N-methyl-D-aspartate (40 mg/kg of BW, ip) administration. The results showed that N-methyl-D-aspartate caused a remarkable increase of lordosis quotient in control rats but not in monosodium L-glutamate-treated rats. Moreover, the possible action site of N-methyl-D-aspartate in the enhancement of receptivity was evaluated by the post-castrational LH rise, pituitary LH release in response to GnRH, and N-methyl-D-aspartate-evoked GnRH releasability. The results revealed that: (a) serum levels of LH in monosodium L-glutamate-treated rats were lower (p <0.01) than those of control rats after ovariectomy; (b) there was no significant difference of pituitary LH release responsiveness to GnRH test between two groups; and (c) N-methyl-D-aspartate-evoked LH release in monosodium L-glutamate-treated rats was similar to that in the control rats. In conclusion, N-methyl-D-aspartate may facilitate the sexual receptivity through stimulating GnRH release. The failure of N-methyl-D-aspartate in enhancing receptivity in monosodium L-glutamate-treated rats is probably due to the cellular damage by monosodium L-glutamate on specific areas responsible for lordosis.
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Storer, R. J., and P. J. Goadsby. "Trigeminovascular nociceptive transmission involves N-methyl-d-aspartate and non-N-methyl-d-aspartate glutamate receptors." Neuroscience 90, no. 4 (June 1999): 1371–76. http://dx.doi.org/10.1016/s0306-4522(98)00536-3.

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Libá, Zuzana, Jitka Hanzalová, Věra Sebroňová, and Vladimír Komárek. "Anti‑N‑ Methyl‑ D‑ Aspartate Receptor Encephalitis." Česká a slovenská neurologie a neurochirurgie 77/110, no. 5 (September 29, 2014): 624–30. http://dx.doi.org/10.14735/amcsnn2014624.

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Collingridge, G. L., J. F. Blake, M. W. Brown, Z. I. Bashir, and E. Ryan. "Involvement of excitatory amino acid receptors in long-term potentiation in the Schaffer collateral–commissural pathway of rat hippocampal slices." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 1084–90. http://dx.doi.org/10.1139/y91-160.

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The present article reviews studies from our laboratory, which have shown that excitatory amino acid receptors of the N-methyl-D-aspartate type are involved in the induction of long-term potentiation in the Schaffer collateral–commissural pathway of rat hippocampal slices. The nature of the excitatory amino acid receptors that mediate the response that is modified by the induction of long-term potentiation is also considered. The mechanism of induction of long-term potentiation is discussed, as are some possible stages that are required for the maintenance of this process. Some new data are presented concerning the ability of N-methyl-D-aspartate to potentiate synaptic transmission and to depress the amplitude of the presynaptic fibre volley. Concerning the potentiation, it is shown that brief (1–2 min) perfusion of slices with N-methyl-D-aspartate is sufficient to potentiate synaptic transmission for at least 3 h. The N-methyl-D-aspartate induced depression of the presynaptic fibre volley is shown to be transient and independent of synaptic transmission.Key words: long-term potentiation, N-methyl-D-aspartate, a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, synaptic plasticity, hippocampus.
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Roginski, Raymond S., Farida Goubaeva, Maya Mikami, Emma Fried-Cassorla, Mohan R. Nair, and Jay Yang. "GRINL1A colocalizes with N-methyl D-aspartate receptor NR1 subunit and reduces N-methyl D-aspartate toxicity." NeuroReport 19, no. 17 (November 2008): 1721–26. http://dx.doi.org/10.1097/wnr.0b013e328317f05f.

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Shibata, Kimihiko, Atsuko Tarui, Natsumi Todoroki, Shinjiro Kawamoto, Shouji Takahashi, Yoshio Kera, and Ryo-hei Yamada. "Occurrence of N-methyl-l-aspartate in bivalves and its distribution compared with that of N-methyl-d-aspartate and d,l-aspartate." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 130, no. 4 (December 2001): 493–500. http://dx.doi.org/10.1016/s1096-4959(01)00455-9.

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ffrench-Mullen, J. M., N. Hori, and D. O. Carpenter. "Receptors for excitatory amino acids on neurons in rat pyriform cortex." Journal of Neurophysiology 55, no. 6 (June 1, 1986): 1283–94. http://dx.doi.org/10.1152/jn.1986.55.6.1283.

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The actions of a variety of agonists and antagonists of the excitatory amino acids on rat pyriform cortex pyramidal neurons were studied in a submerged, perfused brain slice. The order of potency for the agonists, applied by ionophoresis, was kainate greater than quisqualate greater than N-methyl-D-aspartate greater than aspartate = glutamate. The endogenous monosynaptic excitation of pyramidal neurons upon stimulation of the lateral olfactory tract was blocked post-synaptically by DL-2-amino-4-phosphonobutyric acid, although this drug did not consistently block any of the exogenous responses. The synaptic excitation was not blocked, however, by antagonists presumed specific for the quisqualate (glutamate diethyl ester), kainate, (gamma-D-glutamylglycine), or N-methyl-D-aspartate (DL-2-amino-5-phosphonovaleric acid, DL-2-amino-7-phosphonohetaonic acid) receptors. Several antagonists blocked N-methyl-D-aspartate responses at lower concentrations than those to aspartate, and other antagonists distinguished between kainate and quisqualate responses. These results suggest that 1) pyriform neurons have a variety of receptors that have properties somewhat different from those found in other preparations and 2) the endogenous transmitter activates a receptor distinct from those activated by kainate, quisqualate, and N-methyl-D-aspartate.
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Millichap, J. Gordon. "Anti-N-Methyl-D-Aspartate Receptor Encephalitis." Pediatric Neurology Briefs 27, no. 5 (May 1, 2013): 39. http://dx.doi.org/10.15844/pedneurbriefs-27-5-9.

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Williams, Michael, Patricia A. Loo, Deborah E. Murphy, Albert F. Braunwalder, Michael F. Jarvis, and Matthew A. Sills. "The N-Methyl-D-Aspartate Receptor Complex." Journal of Receptor Research 8, no. 1-4 (January 1988): 195–203. http://dx.doi.org/10.3109/10799898809048987.

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Dissertations / Theses on the topic "Methyl aspartate"

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Sim, Neil. "Molecular imaging probes for N-methyl-D-aspartate receptors." Thesis, Durham University, 2014. http://etheses.dur.ac.uk/10816/.

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The non-invasive detection of neuronal transmission is of prime importance in order to understand brain function better. This will aid cognitive neuroscience, as well as medical science, in the early detection of diseased states. Herein, approaches to molecular imaging of the NMDA receptor, a receptor subtype of the excitatory neurotransmitter glutamate, through the use of targeted contrast agents, is described. Initially, a series of NMDA receptor-targeted MRI contrast agents was developed based upon a known competitive NMDA receptor antagonist, appended to an N-linked ‘Gd-DOTA’ core that possesses a fast-exchanging water molecule. Their use as responsive MR imaging probes was evaluated in vitro using a neuronal cell line model, and three contrast agents showed large enhancements in cellular relaxation rates. In order to confirm NMDA receptor localisation, derivatives of the lead compounds were also prepared. The derivatives contained a biotin moiety, which allowed direct visualisation of the cell-surface receptors, after addition of an AvidinAlexaFluor®-488 conjugate. Using these derivatives, the specificity and reversibility (in the presence of glutamate) of binding at the NMDA receptor was demonstrated in living cells using laser scanning confocal microscopy. In an attempt to generate a single-component NMDA receptor-targeted optical imaging agent, a very bright europium complex conjugated to an NMDA receptor-binding moiety was synthesised. Unfortunately, upon incubation with a neuronal cell line model, complex localisation appeared to be dictated by the ligand structure and not by the receptor-binding moiety. One emerging imaging technique with potential applications in neuronal imaging is photoacoustic imaging. Two NMDA receptor-targeted photoacoustic imaging agents were synthesised and their ability to label NMDA receptors assessed in vitro. Finally, preliminary in vivo evaluation of the most promising photoacoustic imaging agent is described.
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Lui, Pik Wa. "Modulation of N-methyl-D-aspartate receptor expression in neuronal cell culture." HKBU Institutional Repository, 2002. http://repository.hkbu.edu.hk/etd_ra/419.

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Bera, Katarzyna D. "Autoantibodies to N-methyl D-aspartate receptors in autoimmune encephalitis." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:6bbda982-ab5c-4982-b23a-0478c689869c.

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N-methyl-D-aspartate receptor (NMDAR) antibody encephalitis is a recently described autoimmune encephalopathy defined by the presence of serum antibodies that bind NMDARs (NMDAR-Abs). NMDAR-Ab encephalitis is a severe, but treatmentresponsive encephalitis with subacute onset. It can be associated with tumours and affects mainly young adults. Patients present with cognitive dysfunction, seizures, psychiatric and sleep disorders and most develop dyskinesias, autonomic instability and reduced consciousness. To explore further the NMDAR-Abs and their potential pathogenicity, a series of in vitro investigations were performed and preliminary attempts at passive transfer of disease. Human embryonic kidney (HEK) cells transfected with the NR1 and NR2B subunits, and live cultured neurons, were used first to detect NMDAR-Ab binding. Immunocytochemistry and ow cytometry demonstrated that binding to transfected HEK cells could be improved when NMDAR were presented in clusters by cotransfection with the postsynaptic density protein PSD-95. The NR1 subunit was identified as the target of NMDAR-Abs, and a novel quantitative assay based on immunoprecipitation of NR1 tagged by fusion with green uorescent protein was developed. Measurement of NMDAR-Ab levels showed that antibody levels corresponded to the clinical disease score within individual patients. Although the purification of full length NR1 was not successful, a secreted N-terminal construct was created and expressed in HEK cells. The binding of NMDAR-Abs was confirmed and this construct will be used for active immunisation in future. To explore pathogenic mechanisms in vitro, the main antibody subclasses were shown to be IgG1 and IgG3. Moreover the patients' autoantibodies, but not healthy control antibodies, were able to activate the complement cascade in vitro in cell lines and primary cultures. Finally, the NMDAR-Abs were shown to bind to primary microglial cultures and to cause morphological changes corresponding to early activation processes after prolonged exposure. The research has developed new assays that could be used for diagnosis and serial studies and revealed new potential mechanisms in NMDAR-Ab encephalitis.
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Paliouras, Grigorios Nikiforos. "Effect of ethanol on the Jak-Stat pathway : is this an NMDA mediated event?" Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79062.

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Alcohol affects many neurochemical processes, causing long-lasting changes in both the adult and developing brain. The Jak-Stat transcriptional activation pathway plays a role in the control of neuronal proliferation, survival and differentiation, but the effects of ethanol on the system have not been fully elucidated. The goal of this project was to define the effects of acute and subchronic ethanol exposure on the expression of proteins in the Jak-Stat pathway, using cultured NG108-15 cells, and in addition, to test the hypothesis that these effects are mediated through the NMDA receptor. I found that ethanol dose-dependently decreased Jak2 and Stat3 following subchronic exposure of NG108-15 in culture. Acute ethanol exposure caused a dose-dependent decrease in Stat3 protein levels. Incubation with MK-801 or ketamine, two noncompetitive NMDA receptor antagonists, or the receptor agonist NMDA, produced dose-dependent decreases in Stat3 protein as well.
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Brothwell, Shona Lindsay Crawford. "Properties of NMDA receptors in Substantia nigra pars compacta dopaminergic neurones." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612352.

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Lin, Raozhou, and 林饒洲. "Kif5b interaction with NMDA receptors regulates neuronal function." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/208429.

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Intracellular transportation is an essential cellular event controlling neuronal development, morphology, function and survival. Kinesin-1 is the molecular motor conveying cargo along microtubule by utilizing the chemical energy from ATP hydrolysis. This motor consists of two heavy chains and two light chains. Both heavy and light chains are responsible for cargo bindings. There are three kinesin-1 heavy chains in eukaryotic cells. Kif5a and Kif5c are neuronal specific, while Kif5b is ubiquitously expressed. Kif5b carries various cargos essential for neuronal functions, and the early embryonic death of Kif5b null mice suggests the importance of Kif5b in vivo. N-methyl-d-aspartate receptors (NMDARs) are glutamate elicited channel, which is permeable to calcium and crucial for synaptic plasticity in the central nervous system. NMDARs are heteromeric assemblies consisting of NR1, NR2 and NR3 subunits. These transmembrane subunits contain three parts. Other than the transmembrane domain, the extracellular domain serves as the ligand binding site while the intracellular domain interacts with various partners regulating downstream signaling and receptor trafficking. Synaptic NMDAR activation regulates synaptic plasticity, while extrasynaptic NMDAR activation leads to excitotoxicity. In this project, I find that kinesin-1 directly interacts with NMDAR subunit, NR1, NR2A and NR2B in vivo. NMDAR colocalizes with kinesin-1 in the cell body and neurites. By GST-pull-down assays with different Kif5b fragments, the cytoplasmic domains of NR1, NR2A and NR2B are found to directly bind with Kif5b via a Kif5b C-terminal region independent of kinesin light chains. To examine the role of Kif5b in NMDAR trafficking, dominant negative Kif5b fragments are expressed in cell lines together with NR1-1a and GFP-NR2B. Overexpression of dominant negative Kif5b significantly disrupts GFP-NR2B forward trafficking and prevents it from entering into Golgi apparatus. Furthermore, the surface NR1 and NR2B levels are significantly reduced whilst the NR2A levels are not affected in Kif5b+/- mice in which the Kif5b protein level is reduced by 50% compared with the wild-type littermates. Consistent with this observation, the NR1 and NR2B levels are decreased in fractions containing synaptosomal membrane but not the one containing only postsynaptic densities, suggesting that the extrasynaptic NMDAR levels are affected in Kif5b+/- mice. NMDARs are highly permeable to calcium while activated, thereby activating neuronal nitric oxide synthases (nNOS) to produce nitric oxide (NO). It is found that NMDA triggered calcium influx is perturbed in Kif5b+/- neurons, while the synaptic NMDA receptor mediated calcium influx is normal. In Kif5b+/- slices, the production of NO reduces significantly. Calcium ionophore, A23187, rescue this NO defect, indicating insufficient supply of calcium as the main contribution to this defect. Therefore, Kif5b-dependent extrasynaptic localization of NMDA receptors mediates calcium influx upon NMDA stimulation and controls NO production. In the summary, above results suggest kinesin-1 as a novel motor involving in NMDA receptor trafficking. This interaction may contribute to the extrasynaptic distribution of NMDARs. By regulating NO production through interaction with NMDARs, Kif5b may mediate neuronal survival in cerebral ischemia and certain aggressive behaviors. This provides a novel target for therapy development against stroke and schizophrenia.
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Yu, Chi Wang. "NMDA receptor mediated toxicity in primary neuronal cultures from rodent cerebral cortex /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202004%20YU.

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Ryan, Tomás John. "Functional investigation of NMDA receptor molecular evolution." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608544.

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Wu, Y. "Extrasynaptic signalling and plasticity mediated by N-Methyl-D-aspartate receptors." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1369568/.

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Synaptic N-Methyl-D-aspartate receptors (NMDARs) are crucial for neural coding and plasticity. However, little is known about the adaptive function of extrasynaptic NMDARs located on the dendritic shaft. Here we find that in CA1 pyramidal neurons backpropagating action potentials (bAPs) recruit shaft NMDARs exposed to ambient glutamate of non-vesicular origin. In contrast, spine NMDARs are "protected" under baseline conditions from such glutamate by perisynaptic transporters: bAP-evoked Ca2+ entry through these receptors can be detected upon synaptic glutamate release or local glutamate uncaging. During theta-burst firing, NMDAR-dependent Ca2+ entry either upregulates or downregulates an h-channel conductance (Gh) of the cell depending on whether synaptic glutamate release is intact or blocked. Gh plasticity in turn regulates dendritic input probed by local glutamate uncaging. Thus, the balance between activation of synaptic and extrasynaptic NMDARs can determine the sign of Gh-dependent plasticity. These results uncover a novel meta-plasticity mechanism potentially important for neural coding and memory formation.
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Yassin, Maged M. I. "N-methyl-D-aspartate, anoxia and glutamate antagonists in mammalian brain." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241524.

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Books on the topic "Methyl aspartate"

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

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Book chapters on the topic "Methyl aspartate"

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Morgan, Michael M., MacDonald J. Christie, Thomas Steckler, Ben J. Harrison, Christos Pantelis, Christof Baltes, Thomas Mueggler, et al. "N-Methyl-D-Aspartate Receptor." In Encyclopedia of Psychopharmacology, 757–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1294.

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Rey, Jose A. "N-Methyl-D-Aspartate (NMDA) Receptors." In Encyclopedia of Clinical Neuropsychology, 2458–59. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1682.

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Rey, Jose A. "N-Methyl-D-Aspartate (NMDA) Receptors." In Encyclopedia of Clinical Neuropsychology, 1778. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1682.

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Rey, Jose A. "N-Methyl-D-Aspartate (NMDA) Receptors." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1682-2.

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Shchepakin, Denis, Leonid Kalachev, and Michael Kavanaugh. "Modeling of N-Methyl-D-Aspartate Receptors." In Trends in Mathematics, 93–98. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-25261-8_14.

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Fisher, George H., and Mara Tsesarskaia. "HPLC Methods for Determination of d-Aspartate and N-methyl-d-Aspartate." In Methods in Molecular Biology, 253–64. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-331-8_16.

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Roberts, Patrick. "N-Methyl-d-Aspartate (NMDA) Receptors, Conductance Models." In Encyclopedia of Computational Neuroscience, 1–3. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_354-1.

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Roberts, Patrick D. "N-Methyl-D-Aspartate (NMDA) Receptors, Conductance Models." In Encyclopedia of Computational Neuroscience, 2100–2101. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_354.

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Hoffman, Paula L., Carolyn S. Rabe, Peter Valverius, Kathleen A. Grant, and Boris Tabakoff. "Genetic Differences in the N-Methyl-d-Aspartate Receptor." In The Genetic Basis of Alcohol and Drug Actions, 353–68. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2067-6_10.

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Tanaka, Keiko. "N-Methyl-D-Aspartate Receptor Antibody-Associated Autoimmune Encephalitis." In Neuroimmunological Diseases, 223–34. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55594-0_14.

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Conference papers on the topic "Methyl aspartate"

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Trajano, Maria Lourdes M., Pediatric Neurologist, and Karenne N. Somera. "N-methyl-d-aspartate Receptor Encephalitis in a Tertiary Hospital: A Case Report." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.496.

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Ohgami, Masatsugu, Nobuhiko Takai, Masahiko Watanabe, Koichi Ando, Akiko Uzawa, and Ryoichi Hirayama. "EFFECT OF N-METHYL-D-ASPARTATE RECEPTOR ANTAGONIST ON RADIATION-INDUCED GUT INJURIES IN MICE." In RAD Conference. RAD Association, 2017. http://dx.doi.org/10.21175/radproc.2017.02.

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Fang, Yuqiang, King W. C. Lai, Catherine Y. Y. Iu, Cathy N. P. Lui, Carmen K. M. Fung, Hung-Wing Li, Ken K. L. Yung, and Ning Xi. "Investigation of N-methyl-D-aspartate induced mechanical behavior of neuroblastoma cells using atomic force microscopy." In 2013 IEEE 13th International Conference on Nanotechnology (IEEE-NANO). IEEE, 2013. http://dx.doi.org/10.1109/nano.2013.6720884.

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Young, Emma C., Helen Sumner, Samantha Decalmer, Lesley Houghton, Ashley A. Woodcock, and Jaclyn Smith. "Does Central Up-regulation Of The N-Methyl-D-Aspartate Receptor Contribute To Cough Reflex Hypersensitivity?" In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5906.

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Golovynska, Iuliia, Tatiana V. Beregova, Tatiana M. Falalyeyeva, Sergii Golovynskyi, Junle Qu, and Tymish Y. Ohulchanskyy. "Combining optical imaging and pharmacological methods to localize N-methyl-D-aspartate glutamate receptors in a stomach wall." In International Conference on Photonics and Imaging in Biology and Medicine. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/pibm.2017.w3a.107.

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Sareen, Nishtha, and Seth Koenig. "Limbic Encephalitis Including Anti-N-Methyl D-Aspartate Encephalitis May Be Under-Recognized In The Medical Intensive Care Unit." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5942.

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Ramos-Bello, D., AN Rangel-Botello, G. Barragan-Pickens Aguilera, TA Luna-Zúñiga, AJ Pedro-Martínez, G. Martínez-Flores, A. Bravo-Oro, and C. Abud-Mendoza. "THU0501 Efficacy and safety of methotrexate as maintenance therapy for children with anti–n-methyl-d-aspartate receptor (NMDAR) encephalitis: experience of a single center." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2726.

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Reports on the topic "Methyl aspartate"

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Patel, Tapan P., Scott C. Ventre, Pallab K. Singh, and David F. Meaney. NR2B-N-Methyl-D-Aspartate Receptors Contribute to Network Asynchrony and Loss of Long-Term Potentiation Following Mild Mechanical Injury In Vitro. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada586145.

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