Relevant bibliographies by topics / NMDA

Academic literature on the topic 'NMDA'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "NMDA"

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Reyes Monreal, Marleni, María Eugenia Pérez Bonilla, Jessica Quintero Pérez, Arturo Reyes Lazalde, and Jorge Flores Hernández. "Lab-NMDAR: simuladores de la electrofisiología básica del receptor NMDA." Acta Universitaria 32 (November 23, 2022): 1–23. http://dx.doi.org/10.15174/au.2022.3597.

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Es necesario el desarrollo de software educativo que permita la implementación de prácticas de laboratorio. En este trabajo se presenta el diseño y desarrollo del programa Lab-NMDAR, constituido por tres simuladores para la enseñanza-aprendizaje de la electrofisiología del receptor NMDA: (1) simulador NMDAR-Bloqueo Mg2+, (2) simulador NMDAR-Glicina y (3) simulador canal único NMDA-Bloqueo Mg2+. El programa se implementó en Visual Basic® para ambiente Windows®. Con estos simuladores el alumno conoce la corriente NMDA, reproduce su dependencia del voltaje, simula su bloqueo por magnesio en registros de corriente macroscópica y en canal único, determina la participación de NMDA y glicina en la activación del receptor NMDA y produce experimentos virtuales dosis-respuesta. El programa es de fácil manejo, se ejecuta en una computadora personal con el mínimo de recursos.
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2

Wang, Ning, Linlin Chen, Nan Cheng, Jingyun Zhang, Tian Tian, and Wei Lu. "Active Calcium/Calmodulin-Dependent Protein Kinase II (CaMKII) Regulates NMDA Receptor Mediated Postischemic Long-Term Potentiation (i-LTP) by Promoting the Interaction between CaMKII and NMDA Receptors in Ischemia." Neural Plasticity 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/827161.

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Active calcium/calmodulin-dependent protein kinase II (CaMKII) has been reported to take a critical role in the induction of long-term potentiation (LTP). Changes in CaMKII activity were detected in various ischemia models. It is tempting to know whether and how CaMKII takes a role in NMDA receptor (NMDAR)-mediated postischemic long-term potentiation (NMDA i-LTP). Here, we monitored changes in NMDAR-mediated field excitatory postsynaptic potentials (NMDA fEPSPs) at different time points following ischemia onsetin vitrooxygen and glucose deprivation (OGD) ischemia model. We found that 10 min OGD treatment induced significant i-LTP in NMDA fEPSPs, whereas shorter (3 min) or longer (25 min) OGD treatment failed to induce prominent NMDA i-LTP. CaMKII activity or CaMKII autophosphorylation displays a similar bifurcated trend at different time points following onset of ischemia bothin vitroOGD orin vivophotothrombotic lesion (PT) models, suggesting a correlation of increased CaMKII activity or CaMKII autophosphorylation with NMDA i-LTP. Disturbing the association between CaMKII and GluN2B subunit of NMDARs with short cell-permeable peptides Tat-GluN2B reversed NMDA i-LTP induced by OGD treatment. The results provide support to a notion that increased interaction between NMDAR and CaMKII following ischemia-induced increased CaMKII activity and autophosphorylation is essential for induction of NMDA i-LTP.
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Chisari, Mariangela, Charles F. Zorumski, and Steven Mennerick. "Cross talk between synaptic receptors mediates NMDA-induced suppression of inhibition." Journal of Neurophysiology 107, no. 9 (May 1, 2012): 2532–40. http://dx.doi.org/10.1152/jn.01145.2011.

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Past research has shown that calcium influx through NMDA receptors (NMDARs) depresses GABAA currents. We examined upstream triggers of this suppression, including involvement of target synaptic GABAA receptors and the NMDARs triggering suppression. In hippocampal neurons, conditioning with 20 μM NMDA for 20 s caused 50% suppression of GABA responses. The suppression was delayed by ∼60 s following NMDA application and persisted for at least 5 min following conditioning. Pharmacology experiments suggested a shift in both the sensitivity to GABA and a loss of functional receptors. NMDA conditioning strongly suppressed inhibitory postsynaptic currents and speeded decay kinetics. Synaptic NMDAR conditioning was necessary to suppress GABA current in pyramidal neurons; extrasynaptic NMDAR activation did not suppress, even when matched to synaptic activation. We found no evidence that specific synaptic NMDAR subunits mediate depression of GABA responses. Although physical colocalization of glutamate and GABAA receptors is mostly likely in extrasynaptic regions, our evidence suggests that NMDAR-induced suppression of GABA responsiveness prominently affects precise, moment-to-moment signaling from synaptic receptors to synaptic receptors.
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Fiorentini, C., and C. Missale. "Oligomeric assembly of dopamine D1 and glutamate NMDA receptors: molecular mechanisms and functional implications." Biochemical Society Transactions 32, no. 6 (October 26, 2004): 1025–28. http://dx.doi.org/10.1042/bst0321025.

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In the striatum, dopamine D1R (D1 receptor) activation potentiates NMDA (N-methyl-D-aspartate) transmission and is required for NMDA-mediated long-term potentiation at corticostriatal synapses. By using a combination of co-immunoprecipitation, pull-out with glutathione S-transferase-fusion proteins and bioluminescence resonance energy transfer, we have reported that the D1R forms a heteromeric complex with the NMDAR (NMDA receptor) and that this mechanism is crucial to recruit the D1R to the postsynaptic density. By using confocal and radioligand-binding assay, we also demonstrated that the interaction with NMDAR abolishes agonist-mediated D1R sequestration, indicating that oligomerization with NMDAR could represent a novel regulatory mechanism modulating D1R cellular trafficking and desensitization.
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Arvanian, Victor L., and Lorne M. Mendell. "Removal of NMDA Receptor Mg2+ Block Extends the Action of NT-3 on Synaptic Transmission in Neonatal Rat Motoneurons." Journal of Neurophysiology 86, no. 1 (July 1, 2001): 123–29. http://dx.doi.org/10.1152/jn.2001.86.1.123.

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NT-3 has previously been reported to enhance AMPA/kainate receptor-mediated synaptic responses in motoneurons via an effect on the N-methyl-d-aspartate (NMDA) receptor. To investigate neurotrophin-3 (NT-3) action further, we measured the NMDA receptor (NMDAR)-mediated synaptic response directly by intracellular recording in motoneurons after blocking AMPA/kainate, GABAA, GABAB and glycine receptor-mediated responses pharmacologically. Two pathways were stimulated, the segmental dorsal root (DR) and the descending ventrolateral fasciculus (VLF). The DR-evoked NMDAR-mediated response in motoneurons of rats younger than 1 wk has two components, the initial one of which is generated monosynaptically. NT-3 strongly potentiated both NMDA components in a rapidly reversible manner. No NMDAR-mediated responses were present at VLF connections and at DR connections in older (1- to 2-wk-old) neonates. Bath-applied NT-3–induced potentiation of the AMPA/kainate receptor-mediated response occurred only at connections that exhibit a synaptic NMDA receptor-mediated response. Reducing Mg2+concentration in the bathing solution restored the NMDAR-mediated response elicited by DR stimulation in older neonates and by VLF throughout the neonatal period (0–2 wk). In low-Mg2+, NT-3 enhanced AMPA/kainate receptor-mediated responses elicited by inputs normally not influenced by NT-3. Thus a major reason for the loss of NT-3 action on AMPA/kainate synaptic responses is the reduced activity of the NMDA receptor due to developing Mg2+ block of NMDA receptor-channel complex as the animal matures, and both can be re-established by reducing Mg2+ concentration in fluid bathing the spinal cord.
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Rivas-Santisteban, Rafael, Iu Raïch, David Aguinaga, Carlos A. Saura, Rafael Franco, and Gemma Navarro. "The Expression of Cellular Prion Protein, PrPC, Favors pTau Propagation and Blocks NMDAR Signaling in Primary Cortical Neurons." Cells 12, no. 2 (January 11, 2023): 283. http://dx.doi.org/10.3390/cells12020283.

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Background: The N-methyl-D-aspartate receptor (NMDAR) is a target in current treatments for Alzheimer’s disease (AD). The human prion protein (PrPC) has an important role in the pathophysiology of AD. We hypothesized that PrPC modulates NMDA signaling, thus being a process associated with Alzheimer’s disease. Methods: NMDAR signaling was characterized in the absence or presence of PrPC in cAMP level determination, mitogen-activated protein kinase (MAPK) pathway and label-free assays in homologous and heterologous systems. Bioluminescence resonance energy transfer was used to detect the formation of NMDAR-PrPC complexes. AXIS™ Axon Isolation Devices were used to determine axonal transport of Tau and pTau proteins in cortical primary neurons in the absence or presence of PrPC. Finally, proximity ligation assays were used to quantify NMDA-PrPC complex formation in neuronal primary cultures isolated from APPSw/Ind transgenic mice, an Alzheimer’s disease model expressing the Indiana and Swedish mutated version of the human amyloid precursor protein (APP). Results: We discovered a direct interaction between the PrPC and the NMDAR and we found a negative modulation of NMDAR-mediated signaling due to the NMDAR-PrPC interaction. In mice primary neurons, we identified NMDA-PrPC complexes where PrPC was capable of blocking NMDAR-mediated effects. In addition, we observed how the presence of PrPC results in increased neurotoxicity and neuronal death. Similarly, in microglial primary cultures, we observed that PrPC caused a blockade of the NMDA receptor link to the MAPK signaling cascade. Interestingly, a significant increase in NMDA-PrPC macromolecular complexes was observed in cortical neurons isolated from the APPSw,Ind transgenic model of AD. Conclusions: PrPC can interact with the NMDAR, and the interaction results in the alteration of the receptor functionality. NMDAR-PrPC complexes are overexpressed in neurons of APPSw/Ind mouse brain. In addition, PrPC exacerbates axonal transport of Tau and pTau proteins.
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Xue, Jiu-Gang, Takayoshi Masuoka, Xian-Di Gong, Ken-Shiung Chen, Yuchio Yanagawa, S. K. Alex Law, and Shiro Konishi. "NMDA receptor activation enhances inhibitory GABAergic transmission onto hippocampal pyramidal neurons via presynaptic and postsynaptic mechanisms." Journal of Neurophysiology 105, no. 6 (June 2011): 2897–906. http://dx.doi.org/10.1152/jn.00287.2010.

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N-methyl-d-aspartate (NMDA) receptors (NMDARs) are implicated in synaptic plasticity and modulation of glutamatergic excitatory transmission. Effect of NMDAR activation on inhibitory GABAergic transmission remains largely unknown. Here, we report that a brief application of NMDA could induce two distinct actions in CA1 pyramidal neurons in mouse hippocampal slices: 1) an inward current attributed to activation of postsynaptic NMDARs; and 2) fast phasic synaptic currents, namely spontaneous inhibitory postsynaptic currents (sIPSCs), mediated by GABAA receptors in pyramidal neurons. The mean amplitude of sIPSCs was also increased by NMDA. This profound increase in the sIPSC frequency and amplitude was markedly suppressed by the sodium channel blocker TTX, whereas the frequency and mean amplitude of miniature IPSCs were not significantly affected by NMDA, suggesting that NMDA elicits repetitive firing in GABAergic interneurons, thereby leading to GABA release from multiple synaptic sites of single GABAergic axons. We found that the NMDAR open-channel blocker MK-801 injected into recorded pyramidal neurons suppressed the NMDA-induced increase of sIPSCs, which raises the possibility that the firing of interneurons may not be the sole factor and certain retrograde messengers may also be involved in the NMDA-mediated enhancement of GABAergic transmission. Our results from pharmacological tests suggest that the nitric oxide signaling pathway is mobilized by NMDAR activation in CA1 pyramidal neurons, which in turn retrogradely facilitates GABA release from the presynaptic terminals. Thus NMDARs at glutamatergic synapses on both CA1 pyramidal neurons and interneurons appear to exert feedback and feedforward inhibition for determining the spike timing of the hippocampal microcircuit.
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Hada, Binika, Mrigendra Bir Karmacharya, So R. Park, and Byung H. Choi. "Low-Intensity Ultrasound Decreases Ischemia-Induced Edema by Inhibiting N-Methyl-d-Aspartic Acid Receptors." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, no. 6 (November 2018): 675–81. http://dx.doi.org/10.1017/cjn.2018.331.

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AbstractBackground: We have previously shown that low-intensity ultrasound (LIUS), a noninvasive mechanical stimulus, inhibits brain edema formation induced by oxygen and glucose deprivation (OGD) or treatment with glutamate, a mediator of OGD-induced edema, in acute rat hippocampal slice model in vitro. Methods: In this study, we treated the rat hippocampal slices with N-methyl-d-aspartic acid (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) to determine whether these different glutamate receptor agonists induce edema. The hippocampal slices were then either sonicated with LIUS or treated with N-methyl-d-aspartic acid receptor (NMDAR) antagonists, namely, MK-801 and ketamine, and observed their effects on edema formation. Results: We observed that treatment with NMDA, an agonist of ionotropic glutamate receptors, induced brain edema at similar degrees compared with that induced by OGD. However, treatment with DHPG, an agonist of metabotropic glutamate receptors, did not significantly induce brain edema. Treatment with the NMDAR antagonists MK-801 or ketamine efficiently prevented brain edema formation by both OGD and NMDA in a concentration-dependent manner. N-Methyl-d-aspartic acid-induced brain edema was alleviated by LIUS in an intensity-dependent manner when ultrasound was administered at 30, 50, or 100 mW/cm2 for 20 minutes before the induction of the edema. Furthermore, LIUS reduced OGD- and NMDA-induced phosphorylation of NMDARs at Y1325. Conclusion: These results suggest that LIUS can inhibit OGD- or NMDA-induced NMDAR activation by preventing NMDAR phosphorylation, thereby reducing a subsequent brain edema formation. The mechanisms by which LIUS inhibits NMDAR phosphorylation need further investigation.
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Myme, Chaelon I. O., Ken Sugino, Gina G. Turrigiano, and Sacha B. Nelson. "The NMDA-to-AMPA Ratio at Synapses Onto Layer 2/3 Pyramidal Neurons Is Conserved Across Prefrontal and Visual Cortices." Journal of Neurophysiology 90, no. 2 (August 2003): 771–79. http://dx.doi.org/10.1152/jn.00070.2003.

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To better understand regulation of N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor complements across the cortex, and to investigate NMDA receptor (NMDAR)-based models of persistent activity, we compared NMDA/AMPA ratios in prefrontal (PFC) and visual cortex (VC) in rat. Whole cell voltage-clamp responses were recorded in brain slices from layer 2/3 pyramidal cells of the medial PFC and VC of rats aged p16–p21. Mixed miniature excitatory postsynaptic currents (mEPSCs) having AMPA receptor (AMPAR)- and NMDAR-mediated components were isolated in nominally 0 Mg2+ ACSF. Averaged mEPSCs were well-fit by double exponentials. No significant differences in the NMDA/AMPA ratio (PFC: 27 ± 1%; VC: 28 ± 3%), peak mEPSC amplitude (PFC: 19.1 ± 1 pA; VC: 17.5 ± 0.7 pA), NMDAR decay kinetics (PFC: 69 ± 8 ms; VC: 67 ± 6 ms), or degree of correlation between NMDAR- and AMPAR-mediated mEPSC components were found between the areas (PFC: n = 27; VC: n = 28). Recordings from older rats (p26–29) also showed no differences. EPSCs were evoked extracellularly in 2 mM Mg2+ at depolarized potentials; although the average NMDA/AMPA ratio was larger than that observed for mEPSCs, the ratio was similar in the two regions. In nominally 0 Mg2+ and in the presence of CNQX, spontaneous activation of NMDAR increased recording noise and produced a small tonic depolarization which was similar in both areas. We conclude that this basic property of excitatory transmission is conserved across PFC and VC synapses and is therefore unlikely to contribute to differences in firing patterns observed in vivo in the two regions.
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Parisi, Eva, Yolanda Almadén, Mercé Ibarz, Sara Panizo, Anna Cardús, Mariano Rodriguez, Elvira Fernandez, and Jose M. Valdivielso. "N-methyl-d-aspartate receptors are expressed in rat parathyroid gland and regulate PTH secretion." American Journal of Physiology-Renal Physiology 296, no. 6 (June 2009): F1291—F1296. http://dx.doi.org/10.1152/ajprenal.90557.2008.

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N-methyl-d-aspartate receptors (NMDAR) are tetrameric amino acid receptors which act as membrane calcium channels. The presence of the receptor has been detected in the principal organs responsible for calcium homeostasis (kidney and bone), pointing to a possible role in mineral metabolism. In the present work, the presence of the receptor was determined in normal parathyroid glands (PTG) by real-time PCR, immunoprecipitation, and immunohistrochemistry. Healthy animals showed a decrease in blood parathyroid hormone (PTH) levels 15 min after the treatment with NMDA. This effect was also observed in animals with high levels of PTH-induced EDTA injection, but not in uremic animals with secondary hyperparathyroidism (2HPT). Normal rat PTG incubated in media with low calcium concentration (0.8 mM CaCl2) showed a decrease in PTH release when NMDA was added to the media. This effect of NMDA was abolished when glands were coincubated with MK801 (a pharmacological blocker of the NMDA channel) or PD98059 (an inhibitor of the ERK-MAPK pathway). Glands obtained from animals with 2HPT showed no effect of NMDA in the in vitro release of PTH, together with a decrease in the expression of NMDAR1. In conclusion, NMDA receptor is present in PTG and is involved in the regulation of the PTH release. The mechanism by which NMDAR exerts its function is through the activation of the MAPK cascade. In uremic 2HPT animals the receptor expression is downregulated and the treatment with NMDA does not affect PTH secretion.
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Dissertations / Theses on the topic "NMDA"

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Garside, Molly. "Interactions of NMDA receptor subunits." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414089.

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De, Jesus Domingues António Miguel. "Novel NMDA receptor splice variants." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/7884.

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Injury to white matter oligodendrocytes is central to several important disorders including cerebral palsy, stroke and multiple sclerosis. Dr. Fern’s group and others have recently shown that NMDA receptors are present on oligodendrocyte processes and mediate injury of these myelinating processes. The pharmacological profile of NMDA receptors present in white matter is quite unique. NMDA receptors are composed of the subunits NR1, NR2A-D and NR3A-B that assemble to form a heterotetrameric complex. Importantly, the subunit composition determines the properties of the receptor complex. Two possibilities were proposed to explain the unusual profile of NMDA receptor-mediated currents in white matter: (1) novel splice variants are expressed in glia and/or (2) the major NMDA receptor complex present is composed of an uncharacterized NMDA receptor subunit stoichiometry. In this PhD project I explored these two hypotheses. NR1, NR2C and NR3A, which are thought to be the major components of NMDA receptors in oligodendrocytes, were cloned from the myelinating rat optic nerve. In addition, all known NMDA receptor subunits were cloned from the neonate rat brain. This analysis revealed that only a subset of NR1 splice variants, those lacking exon 5, is expressed in white matter. I have also cloned NR3B and identified several putative novel splice variants of this subunit in both the optic nerve and the brain. Novel splice variants of NR2B-D were also cloned. Four of these novel NR3B variant were characterized by single cell Ca2+ imaging revealing that the novel variants form function receptors. Furthermore, NR3 subunits influence NMDA receptor glutamate sensitivity and Mg2+ in an NR2-dependent manner. The results here presented reveal a previous uncharacterized wealth of NMDA receptor splice variants which modify NMDA receptor physiology.
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McClean, Mercedes. "NMDA antagonists as antinociceptive agents." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311427.

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Fedele, Laura. "Dysfunctional NMDA receptors in neurological disorders." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10043277/.

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N-methyl-D-aspartate receptors (NMDARs) are ionotropic glutamate receptors that together with a-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) and kainate receptors mediate the vast majority of the fast excitatory neurotransmission in the central nervous system. Given this role, any dysfunction in neurotransmission is likely to have a severe impact on brain physiology. Recent mutations have been reported in NMDAR subunits that cause patients to suffer with a variety of neurodevelopmental disorders. Here, we use multidisciplinary structural modelling, site-directed mutagenesis, electrophysiology and kinetic modelling techniques to investigate how de novo missense mutations in distinct regions of the GluN2B subunit, affect NMDAR function. We predicted that these mutations would have pathophysiological implications and we sought to examine their effects on the cellular and molecular function of NMDARs. We developed a virtually complete 3D model of the human GluN1-GluN2B receptor based on the recently solved crystal structures of the frog and rat NMDARs. The human NMDAR structure locates the positions of the residues of interest, allows deductions about their potential impact on the protein as well as provides insight into the binding sites for Mg2+ and memantine using molecular docking. The functional effects of the missense mutations were first analysed in recombinant NMDARs and revealed gain-of-function and loss-of-function phenotypes, with some lacking an overt phenotype. We selected four most profound phenotypes for study in hippocampal cultured neurons revealing how these mutations can compromise excitatory neurotransmission. In addition, we also explored the therapeutic potential of the FDA-approved channel blocker memantine both in heterologous system as well as on excitatory neurotransmission as a potential therapeutic. Overall, the results suggest strong correlations between the effects of the missense mutations with patient phenotypes. Moreover, the study indicates which pharmacotherapeutic interventions are most likely to be successful as targeted therapies.
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Tang, Tina Tze-Tsang. "Molecular mechanisms regulating NMDA receptor trafficking." Thesis, University of Bristol, 2009. http://hdl.handle.net/1983/684cfaf8-a402-4518-b710-ebc237a3e170.

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Tanguay, Jeffrey Joseph. "The effects of redox agents on NMDA receptor-mediated glutamate release from rat hippocampal slices and on NMDA-mediated toxicity in murine fibroblasts expressing human NMDA receptors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0005/MQ42695.pdf.

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Marwick, Katherine Freda McEwan. "Functional consequences of mutations in GRIN2A and GRIN2B associated with mental disorders." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/23549.

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GRIN2A and GRIN2B encode the GluN2A and GluN2B subunits of the NMDA receptor, a subtype of ionotropic glutamate receptor that displays voltage-dependent block by Mg2+ and a high permeability to Ca2+. These receptors play important roles in synaptogenesis, synaptic transmission and synaptic plasticity, as well as contributing to neuronal loss and dysfunction in several neurological disorders. Recently, individuals with a range of childhood onset epilepsies, intellectual disability and other neurodevelopmental abnormalities have been found to carry heterozygous gene-disrupting or protein-altering point mutations in GRIN2A and GRIN2B. This thesis addresses the hypothesis that these point mutations cause key functional disturbances to NMDA receptor properties that contribute to neurodevelopmental disorders. To test this hypothesis, a group of related mutations were selected for functional assessment in heterologous systems: four missense mutations affecting residues in or near the subunit pore regions, all of which are associated with epilepsy and intellectual disability. To model the impact of gene disrupting mutations in GRIN2A, a preliminary analysis of the functional consequences of GluN2A haploinsufficiency in a genetically modified rat was also performed. Three of the four missense mutations were found to be associated with profound alterations in fundamental NMDA receptor properties: compared to wild type, GluN2AN615K was found to reduce Mg2+ block, GluN2BN615I and GluN2BV618G to cause potentiation by Mg2+, and GluN2AN615K and GluN2BN615I showed reduced conductance. GluN2AR586K was not found to influence the parameters assessed. When GluN2AN615K was expressed alongside wild type subunits in the same NMDA receptor, it was found to have a dominant negative effect. Finally, I established successful gene targeting in a new rat Grin2A knock-out model, and observed that heterozygous neurons had lower GluN2A protein expression and current density, making a good model to study human epilepsies associated with loss of a GRIN2A allele. This thesis provides evidence that three missense mutations in GRIN2A and GRIN2B affect physiologically important properties of the NMDA receptor, and that GluN2A haploinsufficiency influences important neural properties in vitro. This is consistent with these mutations causing disease and highlights these and related mutations as potential therapeutic targets in the future.
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Begg, Alison Jane. "Analysis of NMDA receptor regulated gene expression." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/25053.

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Mutation of two NMDA receptor complex proteins, PSD95 and SynGAP, results in altered phenotypes in NMDA dependent phenomena. As components of the receptor complex, necessary for NMDA mediated signalling, mutation of these proteins may alter pathways that regulate gene expression. Affymetrix microarray analysis of RNA from PSD95-/- forebrain and SynGAP-/- hippocampi, compared to wildtype samples, revealed significant changes, greater than 1.5 fold, in a limited numbers of genes. Of the 12000 transcripts analysed 0.22% were significantly altered in PSD95 mutant tissue and 0.35% were changed in SynGAP mutant tissue. The genes altered in each genotype were distinct, apart from an overlap of 3 genes that were found similarly down regulated in PSD95-/- forebrain and SynGAP-/- hippocampi. These 3 genes, c-fos, nur77 and egr2, are activity dependent and are regulated, in part, through the NMDA receptor. It is possible that changes in gene expression may underlie the electrophysiological and behavioural phenotypes seen PSD95-/- and SynGAP+/- animals. It is likely that the genes altered in each of the mutants represent a subset of the genes regulated by NMDA receptor signalling. To get an understanding of the complete set of genes regulated by the NMDA receptor complex and in vitro method of NMDA receptor stimulation was sought. A primary cultured neuron system was used, allowing NMDA receptor activity to be manipulated by the pharmacological treatment of the culture medium. NMDA and bicuculline treatment of primary cultured cortical neurons proved ineffective methods of inducing activity dependent genes as measured by cfos expression. However, AP5 treatment of primary cultured neurons decreased activity dependent gene expression. Electrophysiological analysis of the cultures revealed that bicuculline treatment had no significant effect on culture activity, where as AP5 treatment caused a significant decrease in neuronal activity.
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Sokolovski, Alexandra. "Sigma-1 Receptors Modulate NMDA Receptor Function." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23652.

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The sigma-1 receptor (σ-1R) is an endoplasmic reticulum (ER) protein that modulates a number of ion channels. It is hypothesized that σ-1Rs activated with agonist translocate to the plasma membrane. The σ-1R potentiates N-methyl-D-aspartate Receptors (NMDARs), important constituents of synaptic plasticity. NMDARs are anchored in the plasma membrane by Postsynaptic Density Protein-95 (PSD-95). The mechanism behind σ-1R modulation of NMDARs is not known. The results of my investigation confirm that σ-1Rs localize extrasomatically. Following σ-1R activation, σ-1R localization to dendrites and postsynaptic densities (PSDs) is upregulated. Unpublished work from our lab has shown that σ-1Rs associate with PSD-95 and NMDARs. Furthermore, immunocytochemistry (ICC) showed σ-1R colocalization with PSD-95 and NMDAR subunits. After σ-1R activation there was significantly increased colocalization between σ-1R, PSD-95, and GluN2B. Overall, this study may have provided insight into the molecular mechanism behind σ-1R modulation of NMDARs, which could have implications in the understanding of synaptic plasticity.
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Bakshi, Deeksha. "The role of NMDA receptors in excitotoxicity." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/43907.

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NMDA receptors are glutamate-gated cation channels named after their prototypical selective agonist NMDA. The channels occur as multiple subtypes, which are formed from interactions between different receptor subunits. NMDA receptor subunits are classified into three families: NR1, NR2A-D, and NR3A, B. NMDA receptors are implicated in HD pathology. During HD, a subset of medium-sized aspiny interneurons in the striatum that co-localize SST, NPY, and the enzyme NOS are selectively spared. In contrast, medium-sized spiny cells that constitute 80 % of all striatal neurons undergo selective neurodegeneration. While it was suggested that the interneurons survive because they lack NMDA receptors, studies including from our lab have shown the presence of NR1 in SST-positive striatal neurons. The finding of NR1 expression and co-localization with SST-positive neurons indicates that NMDA receptor-induced toxicity may be regulated in a receptor-specific manner. Therefore, the present study was conducted to investigate whether NMDA application leads to toxicity that is receptor-specific in HEK293 cells stably transfected with NR1, NR2A, or NR2B. The main findings of this study indicate that NMDA application causes cell death, which varies in intensity and nature, depending upon the NMDA concentration applied, and the receptor-type expressed by the cells. Cells expressing NR1 were found to undergo apoptosis but not necrosis, while cells expressing NR2A/NR2B underwent both apoptosis and necrosis in a receptor-specific manner. In cells expressing NR2A/NR2B, exposure to low concentrations of NMDA resulted in cell death that was predominantly apoptotic. In contrast, exposure to high concentrations of NMDA produced mostly necrosis. In cells expressing NR1, NMDA application caused apoptosis, which exhibited a gradual increase in response to greater concentrations of NMDA. In addition, cell death through apoptosis and/or necrosis was determined to be the greatest at all NMDA concentrations in cells expressing NR2B, followed by those expressing NR2A, and then NR1. Taken together, these results indicate that the activation of receptors formed by NR1, NR2A, or NR2B have different toxic consequences. Thus, the selective neurodegeneration observed during HD may be due to the variation in expression levels of NR1, NR2A, and NR2B between medium-sized aspiny interneurons and medium-sized spiny projection neurons.
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Books on the topic "NMDA"

1

Burnashev, Nail, and Pierre Szepetowski, eds. NMDA Receptors. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7321-7.

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Li, Min. NMDA Receptor Protocols. New Jersey: Humana Press, 1999. http://dx.doi.org/10.1385/1592596835.

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Hashimoto, Kenji, ed. The NMDA Receptors. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49795-2.

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

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

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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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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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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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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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Sirinathsinghji, Dalip J. S., and Ray G. Hill, eds. NMDA Antagonists as Potential Analgesic Drugs. Basel: Birkhäuser Basel, 2002. http://dx.doi.org/10.1007/978-3-0348-8139-5.

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Book chapters on the topic "NMDA"

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Petroianu, Georg, and Peter Michael Osswald. "NMDA-Rezeptorkomplex." In Anästhesie in Frage und Antwort, 147–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-05715-5_50.

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Gritsenko, Karina, Adam Bromberg, and Yury Khelemsky. "NMDA Antagonists." In Pain Medicine, 187–89. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43133-8_52.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "NMDA Receptors." In Encyclopedia of Psychopharmacology, 901. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1401.

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Gardoni, Fabrizio, Flaminio Cattabeni, and Monica Di Luca. "NMDA receptors." In Excitotoxicity in Neurological Diseases, 51–63. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8959-8_4.

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Kumar, Ankit. "NMDA Receptors." In Encyclopedia of Animal Cognition and Behavior, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_174-1.

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Kumar, Ankit. "NMDA Receptors." In Encyclopedia of Animal Cognition and Behavior, 4673–75. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_174.

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Kent, Michael, and David A. Edwards. "NMDA Antagonists." In Hospitalized Chronic Pain Patient, 175–77. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08376-1_32.

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Nguyen, Austin H., and Ariana M. Nelson. "NMDA Blockade." In Anesthesiology In-Training Exam Review, 379–82. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87266-3_72.

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Mori, Hisashi. "Overview of the NMDA Receptor." In The NMDA Receptors, 1–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49795-2_1.

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Papouin, Thomas, and Stéphane H. R. Oliet. "Synaptic and Extra-Synaptic NMDA Receptors in the CNS." In The NMDA Receptors, 19–49. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49795-2_2.

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Conference papers on the topic "NMDA"

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Konthoujam, Bolivia, Satyabrat Malla Bujar Baruah, and Soumik Roy. "Interference Model for NMDA Receptor." In 2020 International Conference on Computational Performance Evaluation (ComPE). IEEE, 2020. http://dx.doi.org/10.1109/compe49325.2020.9200144.

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Ribeiro, Fernanda Cristina Poscai, and Everton Lopes Rodrigues. "Integrative review of the use of NMDA antagonists for TBI treatment." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.190.

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Introduction: The kinetic energy of TBI generates mechanical deformation, which causes release of glutamate, activating ionotropic receptors, principally NMDA receptors, favoring the flow of Ca++ and Na+ into the cell, producing edema. Then, the neurotoxicity generated by glutamate release can be avoided by NMDA antagonists. Objectives: To define if NMDA antagonists are promising for the treatment of TBI by literature analysis and to verify if there are reports of adverse reactions. Methodology: The review utilized the Scielo and Pubmed databases and the keywords used were: NMDA antagonist, Brain edema and Brain injury. The review contains 5 animal tests and 5 clinical studies. Results: Animal tests: CP-98,133 minimized edema, motor damage and is promising in the treatment of memory dysfunction after TBI. The NPS 1506 reduced edema in 24h, without altering the necrosis significantly. Ketamine decreased the volume of necrosis without altering the edema. HU-211 reduced the edema slightly. Clinical studies: NPS 1506 showed a neuroprotective profile and no serius effects. Traxoprodil decreased the mortality rate by 7%. CP-101.606 improved the patient’s condition, without adverse effects. Conclusion: Although NMDA antagonists demonstrate effectiveness in TBI treatment, more studies about adverse effects and efficiency are still needed. Among those analyzed, traxoprodil, NPS-1506 and CP-101.606 still don’t present serious adverse effects and demonstrate effectiveness, proving promising for new studies.
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Sorokina, Elena Gennad’evna, Zhanna B. Semenova, Oksana V. Globa, Olga V. Karaseva, Valentin P. Reutov, Galina A. Ignatieva, Sofya A. Afanasieva, et al. "AUTOIMMUNE RESPONSE OF GLUTAMATE RECEPTORS AND NITRIC OXIDE IN EPILEPSY AND TRAUMATIC BRAIN INJURY." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.23.

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In children with epilepsy and traumatic brain injury (TBI), the content of autoantibodies (aAb) to glutamate receptors (NMDA and AMPA subtypes) and the level of nitric oxide products - nitrothyrosine (NT) and nitrates/ nitrites (NOx) in the blood were studied. The obtained data make it possible to reveal the specificity of damage to AMPA and NMDA subtypes of glutamate receptors in convulsive states and posttraumatic brain injuries. The participation of NO and its products in the development of autoimmune response was revealed.
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Sorita, Atsushi, Joseph P. Mathew, and Phillip Factor. "Anti-NMDA Receptor Encephalitis Resulting In Prolonged Respiratory Failure." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5873.

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Doodnauth, A. V., F. T. Canaday, K. O. Omar, A. A. Mitrokhin, B. Rothschild, and R. L. Arancibia. "A Rare Presentation of Seizure Associated Anti-NMDA Encephalitis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2988.

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Mu, Weihua, and Shixin Ye. "B-factor and Light-induced Allostery in NMDA Receptors." In 2020 5th International Conference on Universal Village (UV). IEEE, 2020. http://dx.doi.org/10.1109/uv50937.2020.9426189.

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Espadinha, Margarida, Jorge Dourado, Rocio Lajarin-Cuesta, Clara Herrera- Arozamena, Lídia Gonçalves, João Lopes, María Rodríguez-Franco, Daniel J. V. A. dos Santos, Cristobal de los Rios, and Maria M. M. Santos. "Bicyclic lactams as potential inhibitors of the NMDA receptor." In 4th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2018. http://dx.doi.org/10.3390/ecmc-4-05631.

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Esber, A., V. Auletta, T. Dakah Abu, D. Bokhua, J. Wickel, D. Brämer, and IB Runnebaum. "Einseitige Adnexektomie zur Therapie bei Anti-NMDA-Rezeptor Enzephalitis." In 64. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe e. V. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1756801.

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Stein, Heike, João Barbosa, Josep Dalmau, and Albert Compte. "NMDA-Receptor Dysfunction Disrupts Serial Biases in Spatial Working Memory." In 2019 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA: Cognitive Computational Neuroscience, 2019. http://dx.doi.org/10.32470/ccn.2019.1304-0.

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Wang, Rubin, Hao Chen, and Zhikang Zhang. "A kinetic model of NMDA ion channel under varying noise." In Second International Symposium on Fluctuations and Noise, edited by Derek Abbott, Sergey M. Bezrukov, Andras Der, and Angel Sanchez. SPIE, 2004. http://dx.doi.org/10.1117/12.547033.

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Reports on the topic "NMDA"

1

Bjorklund, M., J. Schoenwaelder, P. Shafer, K. Watsen, and R. Wilton. Network Management Datastore Architecture (NMDA). RFC Editor, March 2018. http://dx.doi.org/10.17487/rfc8342.

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Clemm, A., Y. Qu, J. Tantsura, and A. Bierman. Comparison of Network Management Datastore Architecture (NMDA) Datastores. RFC Editor, December 2021. http://dx.doi.org/10.17487/rfc9144.

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Peterson, Steven. Treatment Strategies fir the NMDA Component of Organophosphorous Convulsions. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435100.

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Peterson, Steven L., and James Griffith. Treatment Strategies for the NMDA Component of Organophosphorus Convulsions. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412570.

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Peterson, Steven L., and James Griffith. Treatment Strategies for the NMDA Component of Organophosphorus Convulsions. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada418693.

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Lhotka, L., A. Lindem, and Y. Qu. A YANG Data Model for Routing Management (NMDA Version). RFC Editor, March 2018. http://dx.doi.org/10.17487/rfc8349.

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D'Arcangelo, Gabriella. Exploring the Interaction between TSC2, PTEN, and the NMDA Receptor in Animal Models of Tuberous Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada610183.

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D'Arcangelo, Gabriella. Exploring the Interaction Between TSC2, PTEN, and the NMDA Receptor in Animal Models of Tuberous Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada586644.

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Swenson, Robert. NMD BM/C3 Implementation,. Fort Belvoir, VA: Defense Technical Information Center, September 1996. http://dx.doi.org/10.21236/ada319963.

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Perkins, Colin, Aaron Griggs, Jaroslav Flidr, Ron Riley, and Maryann Perez. Next Generation Internet (NGI) Multicast Applications and Architecture (NMAA). Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada411010.

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