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Journal articles on the topic 'Methyl aspartate'

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Published: 4 June 2021
Last updated: 19 February 2022

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1

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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2

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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5

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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6

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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7

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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8

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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9

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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10

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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Hung, Te-Yu, Ning-Hui Foo, and Ming-Chi Lai. "Anti-N-Methyl-d-Aspartate Receptor Encephalitis." Pediatrics & Neonatology 52, no. 6 (December 2011): 361–64. http://dx.doi.org/10.1016/j.pedneo.2011.08.012.

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Chenard, B. L., T. W. Butler, I. A. Shalaby, M. A. Prochniak, B. K. Koe, and C. B. Fox. "Oxindole N-Methyl-D-Aspartate (NMDA) antagonists." Bioorganic & Medicinal Chemistry Letters 3, no. 1 (January 1993): 91–94. http://dx.doi.org/10.1016/s0960-894x(00)80098-0.

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13

Sukiennik, Andrew W., and Richard M. Kream. "N-methyl-d-aspartate receptors and pain." Current Opinion in Anaesthesiology 8, no. 5 (October 1995): 445–49. http://dx.doi.org/10.1097/00001503-199510000-00015.

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Li, Hua, Yan-ke Guo, Ying-lin Cui, and Tao Peng. "Anti-N-methyl-D-aspartate receptor encephalitis." Medicine 97, no. 50 (December 2018): e13625. http://dx.doi.org/10.1097/md.0000000000013625.

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Lim, Sian Y., Ragesh Panikkath, Charoen Mankongpaisarnrung, Ebtesam Islam, Zachary Mulkey, and Kenneth Nugent. "Anti-N-Methyl-d-Aspartate Receptor Encephalitis." American Journal of the Medical Sciences 345, no. 6 (June 2013): 491–93. http://dx.doi.org/10.1097/maj.0b013e3182760e3b.

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Zhao, Bailey, and David G. Nelson. "Anti–N-Methyl-D-Aspartate Receptor Encephalitis." Pediatric Emergency Care 35, no. 9 (September 2019): e159-e161. http://dx.doi.org/10.1097/pec.0000000000001853.

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17

Olney, John W. "Excitotoxicity and N-methyl-D-Aspartate receptors." Drug Development Research 17, no. 4 (1989): 299–319. http://dx.doi.org/10.1002/ddr.430170406.

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Halbert, Roger Kelsey. "Anti-N-Methyl-D-Aspartate Receptor Encephalitis." Journal of Neuroscience Nursing 48, no. 5 (October 2016): 270–73. http://dx.doi.org/10.1097/jnn.0000000000000232.

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19

Dietrich, W. D., O. Alonso, M. Halley, R. Busto, and M. Y. T. Globus. "Intraventricular infusion of N-methyl-d-aspartate." Acta Neuropathologica 84, no. 6 (November 1992): 621–29. http://dx.doi.org/10.1007/bf00227739.

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Dietrich, W. D., M. Halley, O. Alonso, M. Y. T. Globus, and R. Busto. "Intraventricular infusion of N-methyl-D-aspartate." Acta Neuropathologica 84, no. 6 (November 1992): 630–37. http://dx.doi.org/10.1007/bf00227740.

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21

Korinek, M., M. Sedlacek, O. Cais, I. Dittert, and L. Vyklicky. "Temperature dependence of N-methyl-d-aspartate receptor channels and N-methyl-d-aspartate receptor excitatory postsynaptic currents." Neuroscience 165, no. 3 (February 2010): 736–48. http://dx.doi.org/10.1016/j.neuroscience.2009.10.058.

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22

Goh, Kah Kheng, Tzu-Hua Wu, Chun-Hsin Chen, and Mong-Liang Lu. "Efficacy of N-methyl-D-aspartate receptor modulator augmentation in schizophrenia: A meta-analysis of randomised, placebo-controlled trials." Journal of Psychopharmacology 35, no. 3 (January 6, 2021): 236–52. http://dx.doi.org/10.1177/0269881120965937.

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Background: Dysfunction of the N-methyl- D-aspartate glutamate receptor is involved in the putative pathology of schizophrenia. There is growing interest in the potential of N-methyl- D-aspartate receptor modulators to improve the symptoms of schizophrenia, but the evidence for the use of glutamatergic agents for augmenting schizophrenia remains inconclusive. Aims: We conducted a meta-analysis to test the efficacy and safety of N-methyl- D-aspartate receptor modulator supplements in patients with schizophrenia. Methods: Following a systemic search in MEDLINE, Embase, Cochrane and Scopus, 40 double-blinded, randomised, placebo-controlled trials involving 4937 patients with schizophrenia were included in this meta-analysis. The change in the severity of symptoms among patients with schizophrenia was defined as the primary outcome, whereas the safety profiles of the intervention, including the discontinuation rate and adverse events, were defined as secondary outcomes. Results: When added to antipsychotic treatments, N-methyl- D-aspartate receptor modulators improved multiple schizophrenia symptoms, particularly negative symptoms, and had satisfactory side effects and safety profile. Among the seven glutamatergic agents analysed, glycine, D-serine and sarcosine had better treatment profiles than other agents, and NMDA receptor co-agonists, as a group, provided a reduction in schizophrenia symptoms compared to antipsychotic treatments without supplementation. Augmentation with N-methyl- D-aspartate receptor modulators was only effective among patients treated with antipsychotics other than clozapine. Conclusions: The results indicate that N-methyl- D-aspartate receptor modulators, particularly with glycine, D-serine and sarcosine, are more beneficial than the placebo in treating schizophrenia, and the effects extended to both positive and negative symptoms, when augmented with antipsychotics other than clozapine.
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Sharma, Neeru M., Andréa S. Haibara, Kenichi Katsurada, Shyam S. Nandi, Xuefei Liu, Hong Zheng, and Kaushik P. Patel. "Central Ang II (Angiotensin II)-Mediated Sympathoexcitation." Hypertension 77, no. 1 (January 2021): 147–57. http://dx.doi.org/10.1161/hypertensionaha.120.16002.

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Central infusion of Ang II (angiotensin II) has been associated with increased sympathetic outflow resulting in neurogenic hypertension. In the present study, we appraised whether the chronic increase in central Ang II activates the paraventricular nucleus of the hypothalamus (PVN) resulting in elevated sympathetic tone and altered baro- and chemoreflexes. Further, we evaluated the contribution of HIF-1α (hypoxia-inducible factor-1α), a transcription factor involved in enhancing the expression of N-methyl-D-aspartate receptors and thus glutamatergic-mediated sympathetic tone from the PVN. Ang II infusion (20 ng/minute, intracerebroventricular, 14 days) increased mean arterial pressure (126±9 versus 84±4 mm Hg), cardiac sympathetic tone (96±7 versus 75±6 bpm), and decreased cardiac parasympathetic tone (16±2 versus 36±3 versus bpm) compared with saline-infused controls in conscious rats. The Ang II-infused group also showed an impaired baroreflex control of heart rate (−1.50±0.1 versus −2.50±0.3 bpm/mm Hg), potentiation of the chemoreflex pressor response (53±7 versus 30±7 mm Hg) and increased number of FosB-labeled cells (53±3 versus 19±4) in the PVN. Concomitant with the activation of the PVN, there was an increased expression of HIF-1α and N-Methyl-D-Aspartate-type1 receptors in the PVN. Further, Ang II-infusion showed increased renal sympathetic nerve activity (20.5±2.3% versus 6.4±1.9% of Max) and 3-fold enhanced renal sympathetic nerve activity responses to microinjection of N-methyl-D-aspartate (200 pmol) into the PVN of anesthetized rats. Further, silencing of HIF-1α in NG108 cells abrogated the expression of N-methyl-D-aspartate-N-methyl-D-aspartate-type1 induced by Ang II. Taken together, our studies suggest a novel Ang II-HIF-1α-N-methyl-D-aspartate receptor-mediated activation of preautonomic neurons in the PVN, resulting in increased sympathetic outflow and alterations in baro- and chemoreflexes.
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Perouansky, Misha, Eilon D. Kirson, and Yoel Yaari. "Halothane Blocks Synaptic Excitation of Inhibitory Interneurons." Anesthesiology 85, no. 6 (December 1, 1996): 1431–38. http://dx.doi.org/10.1097/00000542-199612000-00025.

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Background Activation of principal hippocampal neurons is controlled by feedforward and feedback inhibition mediated by gamma-aminobutyric acidergic interneurons. The effects of halothane on glutamate receptor-mediated synaptic excitation of inhibitory interneurons have not been reported yet. Methods The effects of halothane on glutamatergic excitatory postsynaptic currents and on spike threshold in visually identified interneurons were studied with tight-seal, whole-cell voltage- and current-clamp recordings in thin slices from adult mouse hippocampus. The excitatory postsynaptic currents were pharmacologically isolated into their N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated components using selective antagonists. Results Halothane (0.37-2.78 mM) reversibly blocked non-N-methyl-D-aspartate and N-methyl-D-aspartate excitatory postsynaptic currents in hippocampal oriens-alveus interneurons. Half-maximal inhibition was observed at similar concentrations (0.59 mM and 0.50 mM, respectively). Halothane inhibited synaptically generated action potentials at concentrations that did not elevate the spike threshold. Conclusions Halothane blocks glutamate receptor-mediated synaptic activation of inhibitory interneurons in the mouse hippocampus.
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Moore, L. E., J. T. Buchanan, and C. R. Murphey. "Localization and interaction of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors of lamprey spinal neurons." Biophysical Journal 68, no. 1 (January 1995): 96–103. http://dx.doi.org/10.1016/s0006-3495(95)80163-3.

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Köhr, G., and I. Mody. "Kindling increases N-methyl-d-aspartate potency at single N-methyl-d-aspartate channels in dentate gyrus granule cells." Neuroscience 62, no. 4 (October 1994): 975–81. http://dx.doi.org/10.1016/0306-4522(94)90336-0.

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Khoodoruth, Mohamed Adil Shah, Widaad Nuzhah Chut-kai Khoodoruth, and Mahmoud Khalil Mahmoud Alshawwaf. "Anti-N-methyl-D-aspartate receptor encephalitis in a young female with subclinical hypothyroidism associated with anti-thyroid peroxidase and anti-thyroglobulin antibodies: A case report." SAGE Open Medical Case Reports 8 (January 2020): 2050313X2094978. http://dx.doi.org/10.1177/2050313x20949780.

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Anti- N-methyl-D-aspartate receptor encephalitis is a life-threatening medical emergency that can be clinically misperceived as Hashimoto’s encephalopathy. We present a case of anti- N-methyl-D-aspartate receptor encephalitis in an otherwise healthy young female with subclinical hypothyroidism without an associated ovarian teratoma. She was first misdiagnosed as Hashimoto’s encephalopathy due to delirium and behavioral changes, seizures, psychosis, and increased amount of thyroid peroxidase and thyroglobulin antibodies in serum. Final diagnosis was established by third week following presentation with the detection of anti- N-methyl-D-aspartate receptor antibodies in her cerebrospinal fluid. After treatment with intravenous immunoglobulin, methylprednisolone, and amisulpride, she recovered significantly with minimal sequelae at 3-week follow-up.
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Koek, Wouter. "N-Methyl-d-Aspartate Antagonists and Drug Discrimination." Pharmacology Biochemistry and Behavior 64, no. 2 (October 1999): 275–81. http://dx.doi.org/10.1016/s0091-3057(99)00055-6.

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Suri, Vinit, Sushma Sharma, Rohan Gupta, SK Sogani, Sunit Mediratta, and Nilesh Jadhao. "Pediatric anti-N methyl D aspartate receptor encephalitis." Journal of Pediatric Neurosciences 8, no. 2 (2013): 120. http://dx.doi.org/10.4103/1817-1745.117841.

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Kovács, Ilona, Éva Szárics, Nina Skuban, and Julianna Kardos. "Deramciclane inhibits N-methyl-D-aspartate receptor function." Brain Research Bulletin 52, no. 1 (May 2000): 39–44. http://dx.doi.org/10.1016/s0361-9230(00)00234-3.

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Cheriyan, John, Rashna D. Balsara, Kasper B. Hansen, and Francis J. Castellino. "Pharmacology of triheteromeric N-Methyl-d-Aspartate Receptors." Neuroscience Letters 617 (March 2016): 240–46. http://dx.doi.org/10.1016/j.neulet.2016.02.032.

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AlShimemeri, Sohaila, Meshari Alsaeed, Joshua Lai, Christopher Uy, and Manouchehr Javidan. "Delayed N-methyl-D-aspartate Receptor Encephalitis Relapse." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 47, no. 2 (December 4, 2019): 264–66. http://dx.doi.org/10.1017/cjn.2019.332.

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Scott, Ori, Lawrence Richer, Karen Forbes, Lyn Sonnenberg, Angela Currie, Myroslava Eliyashevska, and Helly R. Goez. "Anti–N-Methyl-D-Aspartate (NMDA) Receptor Encephalitis." Journal of Child Neurology 29, no. 5 (October 3, 2013): 691–94. http://dx.doi.org/10.1177/0883073813501875.

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Kahn, Ilana, Guy Helman, Adeline Vanderver, and Elizabeth Wells. "Anti–N-Methyl-d-Aspartate (NMDA) Receptor Encephalitis." Journal of Child Neurology 32, no. 2 (November 22, 2016): 243–45. http://dx.doi.org/10.1177/0883073816675557.

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Anti– N-methyl-d-aspartate receptor (NMDAR) encephalitis has been shown to be a treatable form of autoimmune encephalitis, but there remains no standardized approach to immunotherapy. We designed an anonymous survey sent to members of the Child Neurology Society to identify the current practices among child neurologists. A total of 151 pediatric neurologists responded to the survey. With these responses we were able to highlight areas of practice uniformity, including first-line treatment with intravenous immunoglobulin and intravenous methylprednisone and initiation of disease-modifying therapy with rituximab alone. The survey also identifies existing gaps in knowledge, specifically, when to add disease-modifying therapy and how long to continue therapy. We propose that the areas of agreement can be used as a step toward establishing standard treatment guidelines and research protocols directed at evidence-based clinical trials.
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Shen, Yin, Xiao-Ling Liu, and Xiong-Li Yang. "N-Methyl-D-Aspartate Receptors in the Retina." Molecular Neurobiology 34, no. 3 (2006): 163–80. http://dx.doi.org/10.1385/mn:34:3:163.

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McIlhinney, R. A. J., E. Philipps, B. Le Bourdelles, S. Grimwood, K. Wafford, S. Sandhu, and P. Whiting. "Assembly of N-methyl-d-aspartate (NMDA) receptors." Biochemical Society Transactions 31, no. 4 (August 1, 2003): 865–68. http://dx.doi.org/10.1042/bst0310865.

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The N-methyl-d-aspartate receptor (NMDAR) requires both NR1 and NR2 subunits to form a functional ion channel. Despite the recent advances in our understanding of the contributions of these different subunits to both the function and pharmacology of the NMDAR, the precise subunit stoichiometry of the receptor and the regions of the subunits governing subunit interactions remain unclear. Since NR2 subunits are not transported to the cell surface unless they associate with NR1 subunits, cell-surface expression of NR2A can be used to monitor the association of the different subunits in cells transfected with N- and C-terminally truncated NR1 subunits. By combining measurements of cell-surface expression of NR2A with co-immunoprecipitation experiments, and by using Blue Native gel electrophoresis to determine the oligomerization status of the subunits, we have shown that regions of the N-terminus of NR1 are critical for subunit association, whereas the truncation of the C-terminus of NR1 before the last transmembrane region has no effect on the association of the subunits. Evidence from the Blue Native gels, sucrose-gradient centrifugation and size exclusion of soluble NR1 domains suggests that NR1 subunits alone can form stable dimers. Using a cell line, which can be induced to express the NMDAR following exposure to dexamethasone, we have shown that NMDARs can be expressed at the cell surface within 5 h of the recombinant gene induction, and that there appears to be a delay between the first appearance of the subunits and their stable association.
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Mehta, Sachin, Piotr Szawarski, Orlando B. Swayne, Dimitri M. Kullmann, and David CJ Howell. "N-methyl-D-aspartate receptor antibody-mediated encephalitis." British Journal of Hospital Medicine 73, no. 8 (August 2012): 472–73. http://dx.doi.org/10.12968/hmed.2012.73.8.472.

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Zhang, Xiong, and Chu Chen. "Astrocytes express functional N-methyl-D-aspartate receptors." Cell Biology International 32, no. 3 (March 2008): S67. http://dx.doi.org/10.1016/j.cellbi.2008.01.284.

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39

Lerma, Juan. "Spermine regulates N-methyl-d-aspartate receptor desensitization." Neuron 8, no. 2 (February 1992): 343–52. http://dx.doi.org/10.1016/0896-6273(92)90300-3.

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40

Cotman, C. W., J. W. Geddes, R. J. Bridges, and D. T. Monaghan. "N-methyl-D-aspartate receptors and Alzheimer's disease." Neurobiology of Aging 10, no. 5 (September 1989): 603–5. http://dx.doi.org/10.1016/0197-4580(89)90144-9.

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41

Murdie, Douglas, Gary Cooney, and John Ferguson. "Seronegative Anti–N-Methyl-D-Aspartate Receptor Encephalitis." Biological Psychiatry 79, no. 9 (May 2016): e67-e68. http://dx.doi.org/10.1016/j.biopsych.2015.05.024.

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42

Daida, Atsuro, Shin-ichiro Hamano, Satoru Ikemoto, Yuko Hirata, Ryuki Matsuura, Reiko Koichihara, Daiju Oba, and Hirofumi Ohashi. "Use of Perampanel and a Ketogenic Diet in Nonketotic Hyperglycinemia: A Case Report." Neuropediatrics 51, no. 06 (March 16, 2020): 417–20. http://dx.doi.org/10.1055/s-0040-1708536.

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Abstract Background Nonketotic hyperglycinemia is a severe form of early onset epileptic encephalopathy caused by disturbances in the glycine cleavage system; the neurological damage is mainly attributed to overstimulation of the N-methyl-D-aspartate receptor. Case The patient presented with a severe form of nonketotic hyperglycinemia and experienced frequent epileptic spasms and focal seizures, which were resistant to vigabatrin, adrenocorticotropic hormone therapy, and combined dextromethorphan and sodium benzoate treatments. By 9 months of age, perampanel reduced epileptic spasms by >50%. At 14 months of age, the ketogenic diet markedly reduced focal seizures and glycine levels in the cerebrospinal fluid. Conclusion Perampanel reduced fast excitatory neuronal activity, which was induced by an α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor, followed by prolonged electrical depolarizations due to an N-methyl-D-aspartate receptor. Furthermore, the ketogenic diet may have modulated the excessive neurotoxic cascade through the N-methyl-D-aspartate receptor. Perampanel and ketogenic diet were effective for seizure control in our patient.
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43

Liang, Yiru, Yu Zhang, Yujing Hu, Bo Xia, Xianfu Lin, and Qi Wu. "Lipase-catalyzed synthesis of chiral poly(ester amide)s with an alternating sequence of hydroxy acid and l/d-aspartate units." Polymer Chemistry 9, no. 12 (2018): 1412–20. http://dx.doi.org/10.1039/c7py01936j.

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Alternating poly(hydroxyhexanoic acid-alt-l/d-β-aspartate)s with α-benzyl or α-methyl ester side groups were prepared via the enzymatic polycondensation of N-(6-hydroxyhexanoyl) l/d-aspartate diesters.
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44

Dempsey-Jones, Harriet, Susann Steudte-Schmiedgen, Michael Browning, Tamar R. Makin, Marcella L. Woud, Catherine J. Harmer, Juergen Margraf, and Andrea Reinecke. "Human perceptual learning is delayed by the N-methyl-D-aspartate receptor partial agonist D-cycloserine." Journal of Psychopharmacology 35, no. 3 (February 11, 2021): 253–64. http://dx.doi.org/10.1177/0269881120986349.

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Background: The optimisation of learning has long been a focus of scientific research, particularly in relation to improving psychological treatment and recovery of brain function. Previously, partial N-methyl-D-aspartate agonists have been shown to augment reward learning, procedural learning and psychological therapy, but many studies also report no impact of these compounds on the same processes. Aims: Here we investigate whether administration of an N-methyl-D-aspartate partial agonist (D-cycloserine) modulates a previously unexplored process – tactile perceptual learning. Further, we use a longitudinal design to investigate whether N-methyl-D-aspartate-related learning effects vary with time, thereby providing a potentially simple explanation for apparent mixed effects in previous research. Methods: Thirty-four volunteers were randomised to receive one dose of 250 mg D-cycloserine or placebo 2 h before tactile sensitivity training. Tactile perception was measured using psychophysical methods before and after training, and 24/48 h later. Results: The placebo group showed immediate within-day tactile perception gains, but no further improvements between-days. In contrast, tactile perception remained at baseline on day one in the D-cycloserine group (no within-day learning), but showed significant overnight gains on day two. Both groups were equivalent in tactile perception by the final testing – indicating N-methyl-D-aspartate effects changed the timing, but not the overall amount of tactile learning. Conclusions: In sum, we provide first evidence for modulation of perceptual learning by administration of a partial N-methyl-D-aspartate agonist. Resolving how the effects of such compounds become apparent over time will assist the optimisation of testing schedules, and may help resolve discrepancies across the learning and cognition domains.
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van der Doef, Thalia F., Sandeep SV Golla, Pieter J. Klein, Gisela M. Oropeza-Seguias, Robert C. Schuit, Athanasios Metaxas, Ellen Jobse, et al. "Quantification of the novel N-methyl-d-aspartate receptor ligand [11C]GMOM in man." Journal of Cerebral Blood Flow & Metabolism 36, no. 6 (October 5, 2015): 1111–21. http://dx.doi.org/10.1177/0271678x15608391.

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[11C]GMOM (carbon-11 labeled N-(2-chloro-5-thiomethylphenyl)- N′-(3-[11C]methoxy-phenyl)- N′-methylguanidine) is a PET ligand that binds to the N-methyl-d-aspartate receptor with high specificity and affinity. The purpose of this first in human study was to evaluate kinetics of [11C]GMOM in the healthy human brain and to identify the optimal pharmacokinetic model for quantifying these kinetics, both before and after a pharmacological dose of S-ketamine. Dynamic 90 min [11C]GMOM PET scans were obtained from 10 subjects. In six of the 10 subjects, a second PET scan was performed following an S-ketamine challenge. Metabolite corrected plasma input functions were obtained for all scans. Regional time activity curves were fitted to various single- and two-tissue compartment models. Best fits were obtained using a two-tissue irreversible model with blood volume parameter. The highest net influx rate (Ki) of [11C]GMOM was observed in regions with high N-methyl-d-aspartate receptor density, such as hippocampus and thalamus. A significant reduction in the Ki was observed for the entire brain after administration of ketamine, suggesting specific binding to the N-methyl-d-aspartate receptors. This initial study suggests that the [11C]GMOM could be used for quantification of N-methyl-d-aspartate receptors.
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Ruiz-García, Josefina, and María del Carmen Iznaola Muñoz. "Anti-N-Methyl-D-Aspartate receptor encephalitis and ovarian teratoma." ACTUALIDAD MEDICA 101, no. 799 (December 31, 2016): 208–10. http://dx.doi.org/10.15568/am.2016.799.ao01.

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Sakaguchi, T., M. Okada, M. Kuno, and K. Kawasaki. "Dual mode ofN-methyl-d-aspartate-induced neuronal death in hippocampal slice cultures in relation toN-methyl-d-aspartate receptor properties." Neuroscience 76, no. 2 (January 1997): 411–23. http://dx.doi.org/10.1016/s0306-4522(96)00403-4.

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Mehta, AK, S. Halder, N. Khanna, OP Tandon, and KK Sharma. "Antagonism of stimulation-produced analgesia by naloxone and N-methyl-D-aspartate: role of opioid and N-methyl-D-aspartate receptors." Human & Experimental Toxicology 31, no. 1 (July 29, 2011): 51–56. http://dx.doi.org/10.1177/0960327111417908.

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Hu, Bin, and Charles W. Bourque. "Functional N-Methyl-D-Aspartate and Non-N-Methyl-D-Aspartate Receptors are Expressed by Rat Supraoptic Neurosecretory Cells in vitro." Journal of Neuroendocrinology 3, no. 5 (October 1991): 509–14. http://dx.doi.org/10.1111/j.1365-2826.1991.tb00311.x.

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Yeh, G. C., D. W. Bonhaus, J. V. Nadler, and J. O. McNamara. "N-methyl-D-aspartate receptor plasticity in kindling: quantitative and qualitative alterations in the N-methyl-D-aspartate receptor-channel complex." Proceedings of the National Academy of Sciences 86, no. 20 (October 1, 1989): 8157–60. http://dx.doi.org/10.1073/pnas.86.20.8157.

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