Cessation of chronic ethanol consumption can increase the sensitivity of the brain to excitotoxic damages. Cannabinoids have been proposed as neuroprotectants in different models of neuronal injury, but their effect have never been investigated in a context of excitotoxicity after alcohol cessation. Here we examined the effects of the pharmacological activation/inhibition of the endocannabinoid system in an in vitro model of chronic ethanol exposure and withdrawal followed by an excitotoxic challenge. Ethanol withdrawal increased N-methyl-D-aspartate (NMDA)-evoked neuronal death, probably by altering the ratio between GluN2A and GluN2B NMDA receptor subunits. The stimulation of the endocannabinoid system with the cannabinoid agonist HU-210 decreased NMDA-induced neuronal death exclusively in ethanol-withdrawn neurons. This neuroprotection could be explained by a decrease in NMDA-stimulated calcium influx after the administration of HU-210, found exclusively in ethanol-withdrawn neurons. By contrast, the

The phosphorylation of Amyloid Precursor Protein (APP) at Thr668 plays a key role in APP metabolism that is highly relevant to AD. The c-Jun-N-terminal kinase (JNK), glycogen synthase kinase-3β (GSK-3β) and cyclin-dependent kinase 5 (Cdk5) can all be responsible for this phosphorylation. These kinases are activated by excitotoxic stimuli fundamental hallmarks of AD. The exposure of cortical neurons to a high dose of NMDA (100 μM) for 30-45 led to an increase of P-APP Thr668. During NMDA stimulation APP hyperphosphorylation has to be assigned to GSK-3β activity, since addition of L803-mts, a substrate competitive inhibitor of GSK-3β reduced APP phosphorylation induced by NMDA. On the contrary, inhibition of JNK and Cdk5 with D-JNKI1 and Roscovitine respectively did not prevent NMDA-induced P-APP increase. These data show a tight connection, in excitotoxic conditions, between APP metabolism and the GSK-3β signaling pathway.

Stroke is an acute brain health issue which causes neuronal damage which has currently no safe and effective neuroprotective treatment approaches. Immediately following a stroke, the brain tissue loses blood perfusion and the center of the infarct deteriorates quickly. This then causes milder ischemia and many brain cells or neurons will result in delayed death which can take up to several hours or even days. Research studies show that the mechanism of cell death is mainly NMDA receptor-dependent excitotoxicity. In ischemic areas, extracellular glutamate levels increase while preventing glutamate release, synaptic activity, or NMDAR activation which was capable of limiting cell death in a variety of stroke models. Thus, preventing excitotoxicity is an important treatment approach for reducing brain damage and improving patient outcome measures following a stroke, and this has definitely encouraged extensive efforts towards developing NMDA receptor-based stroke treatment approaches over the last ...

INSERM - U. 254 et Universite de Montpellier II, CHR Hopital St. Charles, France. An excitatory amino acid, possibly L-glutamate, which probably acts as a neurotransmitter at the inner hair cell-afferent fiber synapses in the cochlea. In the present study, we have used an electrophysiological approach to investigate at this level the presence of a major type of excitatory amino acid receptor, namely the glutamatergic receptor for which N-methyl-D-aspartate is a selective agonist. Our results show that, when N-methyl-D-aspartate and the antagonist 2-amino-5-phosphonovalerate are perfused through the perilymphatic scalae, they induced, by different mechanisms, a significant reduction of the amplitude of the compound action potential and an increase of the N1 latency, both predominant at high intensity tone burst stimulations. No significant difference was found in the presence or absence of Mg2+ in the artificial perilymph used as a vehicle. A further slight N-methyl-D-aspartate-induced decrease ...

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Bicuculline methiodide (BIC-Mel) (10-100 microM) altered the kinetics of N-methyl-D-aspartate (NMDA) responses in single-channel and whole-cell recordings. The principal effect of BIC-Mel (10-100 microM) on NMDA channels was a dose-dependent decrease in mean channel open time (tau o), accompanied by the introduction of a new closed time (tau B) of 14.0 +/- 3.5 msec (mean +/- standard deviation; n = 14) in closed time distributions, which was independent of BIC-Mel concentration. BIC-Mel (10-100 microM) increased the frequency of NMDA channel opening in a dose-dependent manner, offsetting the decrease in tau o, such that the total time spent in the open state per minute was unchanged, and thus the total charge/min through NMDA channels was unchanged. Similarly, the amplitudes of NMDA whole-cell current responses were not noticeably affected by 10-80 microM BIC-Mel, even though power spectra density analysis of the whole-cell NMDA-stimulated noise revealed changes in the underlying channel ...

In addition to its functions as a neuronal messenger molecule, nitric oxide (NO) has also been implicated in playing a major role in ischemic damage and glutamate neurotoxicity. Using primary cortical cultures from transgenic neuronal NO synthase (NOS) null (nNOS-) mice, we definitively establish NO as a mediator of NMDA and hypoxic neurotoxicity. Neurotoxicity elicited by NMDA is markedly attenuated in nNOS- cortical cultures compared with wild-type cultures. The NOS inhibitor nitro-L-arginine is neuroprotective in wild-type but not nNOS- cultures, confirming the role of nNOS-derived NO in glutamate neurotoxicity. Confirming that the nNOS- cultures lack NMDA-stimulated nNOS activity, NMDA did not stimulate the formation of cGMP in nNOS- cultures, but markedly elevates cGMP in wild-type cultures. Both wild- type and nNOS- cultures are sensitive to toxicity induced by NO donors, indicating that pathways stimulated by NO that result in neuronal cell death are still intact in the transgenic mice. ...

The present study documents that NMDA channel activity may be upregulated or downregulated by remote NMDA receptors, depending on the amount of Na+ and Ca2+ influx. If Na+ influx is blocked, Ca2+ influx induced by the activation of remote NMDA receptors may inhibit NMDA channel gating. However, this inhibitory effect can be overcome by an increase in [Na+]i of ,5 mm. Thus there may be a functional Na+-Ca2+ interaction in the regulation of NMDA channels.. Further detailed investigations document that the effects of Na+ and Ca2+ influx on NMDA channel gating during the activation of remote NMDA receptors cannot be explained simply by an algebraic sum of two opposite effects growing monotonically, because (1) Ca2+ influx required to downregulate NMDA receptors under the condition of no Na+ influx is found to be much smaller than that during NMDA receptor activation under normal conditions; (2) a modest Na+ influx, which produces a much smaller increase in [Na+]i than that during NMDA receptor ...

NMDA receptors are glutamate- and glycine-gated channels that mediate fast excitatory transmission in the central nervous system and are critical to synaptic development, plasticity and integration. They have a rich complement of modulatory sites, which represent important pharmacologic targets. Ifenprodil is a well-tolerated NMDA receptor inhibitor; it is selective for GluN2B-containing receptors; and has neuroprotective effects. The mechanism by which ifenprodil inhibits NMDA receptor responses is not fully understood. The inhibition is incomplete and non-competitive with other known NMDA receptor agonists or modulators, although reciprocal effects have been reported between ifenprodil potency and that of extracellular ligands including glutamate, glycine, zinc, protons and polyamines. Recently, structural studies revealed that ifenprodil binds to a unique site at the interface between the extracellular N-termini of GluN1 and GluN2B subunits supporting the view that interactions with other ...

Expressions of N-methyl-D-aspartate receptors NR2A and NR2B subunit proteins in normal and sulfite-oxidase deficient rats hippocampus: effect of exogenous sulf

Routes of NMDA- and K(+)-stimulated calcium entry in rat cerebellar granule cells.: The routes of Ca2+ entry in response to N-methyl-D-aspartate (NMDA) and K+ d

Erythromycin is used to treat many kinds of infections. Erythromycins are also used to prevent strep infections in patients with a history of rheumatic heart disease who may be allergic to penicillin.. ...

TY - JOUR. T1 - Effect of N-methyl-D,L-aspartate (NMA) on gonadotropin-releasing hormone (GnRH) gene expression in male mice. AU - Wu, T. J.. AU - Gibson, Marie J.. AU - Roberts, James L.. N1 - Funding Information: This project was supported by DK39029 (JLR), NS20335 (MJG) and T32-DK07645 (TJW). The authors wish to thank Dr. Areta Dobrjansky for assistance with the LH RIA, and Dr. Yuhua Sun for helpful discussions and Ms. Alice Elste for reading the manuscript.. PY - 2000/4/17. Y1 - 2000/4/17. N2 - The glutamate analog N-methyl-D,L-aspartate (NMA) affects the regulation of GnRH and LH release in mammals. Several laboratories have reported a rapid and transient increase in GnRH mRNA levels of male rats after NMA injection. Studies employing the simultaneous measurements of nuclear GnRH primary transcript RNA, a reflection of gene transcription, and GnRH mRNA suggest that NMAs effect on GnRH gene expression in the rat is likely due to post-transcriptional regulation. Despite the increasingly ...

Purpose: : During NMDA-induced cell death in the neural retina, there is an elevation of the nuclear isoform of CaMKIIα (CaMKIIαB). This result leads to the question of how CaMKIIαB might be involved in either a cell death or cell survival pathway, for example, in retinal ganglion cells (RGCs). The purpose of this study is to investigate if CaMKIIα regulates BDNF expression in RGCs. Methods: : Highly purified RGCs or dissociated retinal cells were obtained from P6-8 SD rat eyes and treated with glutamate (200-1000uM) for the indicated times. Glutamate cytotoxicity on RGCs and localization of CaMKIIα was determined by cell counting and immunostaining, respectively. To identify the role of CaMKIIα in regulating BDNF expression, CaMKIIαB expression vector was constructed and over-expressed in cells of the RGC-5 cell line, and cell viability was assayed. Specific siRNAs to knock down CaMKIIαB or CaMKIIα were then tested in CaMKIIαB-transfected or non-transfected RGC-5 cells. The siRNAs ...

N-Methyl-D-aspartic acid or N-Methyl-D-aspartate (NMDA) is an amino acid derivative that acts as a specific agonist at the NMDA receptor mimicking the action of glutamate, the neurotransmitter which normally acts at that receptor. Unlike glutamate, NMDA only binds to and regulates the NMDA receptor and has no effect on other glutamate receptors (such as those for AMPA and kainate). NMDA receptors are particularly important when they become overactive during withdrawal from alcohol as this causes symptoms such as agitation and, sometimes, epileptiform seizures. NMDA is a water-soluble synthetic substance that is not normally found in biological tissue. It was first synthesized in the 1960s. NMDA is an excitotoxin (it kills nerve cells by over-exciting them); this trait has applications in behavioral neuroscience research. The body of work utilizing this technique falls under the term lesion studies. Researchers apply NMDA to specific regions of an (animal) subjects brain or spinal cord and ...

Our results support the hypothesis that cholesterol status of neurons is crucial for excitotoxicity since we found that inhibition of cholesterol synthesis prevents NMDA-induced neuronal death. Two different inhibitors of cholesterol synthesis, the inhibitor of Δ14-Δ7 reductase AY9944 and the inhibitor of HMGCoA reductase simvastatin, protect from excitotoxic cell death in pure neuronal cultures (Figures 2 and 3⇑). Both compounds inhibited cholesterol synthesis, but contrary to simvastatin, AY4499 does not inhibit isoprenylation or farnesylation.22 In agreement with results previously reported,10 we found that simvastatin protected against excitotoxicity at nanomolar concentrations and required pretreatments ,2 days to provide neuroprotection.10,11 These 2 observations suggest that the effect of simvastatin on neuroprotection relays on its effect on cholesterol synthesis, because the inhibition of prenylation by statins occurs at higher concentrations and with shorter exposure times than ...

Dai H, Fu Q, Shen Y, Hu W, Zhang Z, Timmerman H, Leurs R, Chen Z. The histamine H3 receptor antagonist clobenpropit enhances GABA release to protect against NMDA-induced excitotoxicity through the cAMP/protein kinase A pathway in cultured cortical neurons. European Journal of Pharmacology. 2007 Jun 1;563(1-3):117-23. PMID 17350613 ...

We report here that brief exposure to 5-50 μM extracellular zinc, comparable to the concentrations estimated to be released normally into synaptic clefts (4), selectively enhanced the phosphorylation of neuronal Src at tyrosine 220 in the SH2 domain, without affecting tyrosine phosphorylation of Fyn. This phosphorylation was accompanied by increases in Src activity, NMDA receptor phosphorylation, and NMDA receptor function (current and excitotoxicity). Drawing on key earlier studies as well as present measurements of [Na+]i in neurons exposed to zinc, we propose that the ability of zinc to induce this up-regulation of Src activity and NMDA receptor function is mediated by inhibition of plasma membrane Na+/K+ ATPase and elevated [Na+]i. Although low concentrations of zinc can potentiate current mediated by certain homomeric NMDA receptor subunit 1 (NR1) splice variants, zinc potentiation of more physiological heteromeric NR1/NR2 receptors was not previously observed (70, 71).. No change in the ...

After an excitotoxic lesion in the postnatal cortex, glial NF-κB is consistently activated at 10 hours after injury, showing its peak at day 1.4 Therefore, when triflusal is orally administered 8 hours after the NMDA injection, it preferentially targets NF-κB induced in glial cells, as the inducible neuronal NF-κB is starting to decrease when triflusal reaches the brain. Glial NF-κB is probably induced by injury-related signals that occur in the degenerating area. They may include reactive oxygen species, produced in excitotoxically damaged cells,44 and the proinflammatory cytokines interleukin-1β and tumor necrosis factor-α, which are expressed by neurons and glial cells in this excitotoxic lesion model, showing a peak of expression at 10 hours after injury.45 On activation, NF-κB translocates to the cell nucleus and modulates the expression of several genes implicated in the development of the glial and inflammatory responses. Target genes containing a NF-κB-binding site include the ...

TY - JOUR. T1 - Na+ occupancy and Mg2+ block of the N-methyl-D-aspartate receptor channel. AU - Zhu, Yongling. AU - Auerbach, Anthony. PY - 2001. Y1 - 2001. N2 - The effect of extracellular and intracellular Na+ on the single-channel kinetics of Mg2+ block was studied in recombinant NR1-NR2B NMDA receptor channels. Na+ prevents Mg2+ access to its blocking site by occupying two sites in the external portion of the permeation pathway. The occupancy of these sites by intracellular, but not extracellular, Na+ is voltage-dependent. In the absence of competing ions, Mg2+ binds rapidly (,108 M-1s-1, with no membrane potential) to a site that is located 0.60 through the electric field from the extracellular surface. Occupancy of one of the external sites by Na+ may be sufficient to prevent Mg2+ dissociation from the channel back to the extracellular compartment. With no membrane potential; and in the absence of competing ions, the Mg2+ dissociation rate constant is ,10 times greater than the Mg2+ ...

N-methyl-D-aspartate receptors activate transcription of c-fos and NGFI-A by distinct phospholipase A2-requiring intracellular signaling pathways.

Lately there has been alot of hype around ketamine for the treatement of depression. There has also been some talks regarding NMDA receptor agonists...

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Background Constitutive and regulated internalization of cell surface proteins has been extensively investigated. The regulated internalization has been characterized as a principal mechanism for...

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Title: New Peptidic Neuroprotectants Against NMDA Neurotoxicity: Syntheses and Biological Evaluations of Linear Complestatin Analogs. VOLUME: 5 ISSUE: 2. Author(s):Ho-Joon Park, Seung-Woo Kim, Young-Gyun Shin, Yun-Jung Kim, Ja-Kyeong Lee, Suk Bin Kong and Sung-Hwa Yoon. Affiliation:Department of Molecular Science and Technology, Ajou University, Suwon, 443-749 South Korea.. Keywords:NMDA, Neurotoxicity, Complestatin, LDH release, 3,5-dichloro-4-hydroxyphenylglycine. Abstract: Linear peptide analogs of complestatin were synthesized via solid phase peptide synthesis and tested in vitro as inhibitors against N-methyl-D-aspartic acid (NMDA) neurotoxicity as possible new peptidic neuroprotectants. While none of the analogs were as potent as the parent compound (IC50 = 2.5 μM), hexamer 11c and heptamer 1c, which contain all D-amino acids, showed modestly potent neuroprotective effects with IC50 values of 23.8 μM and 22.5 μM, respectively. The results indicate that the bicyclic ring structure of ...

DHEA, together with DHEAS, is the most abundant steroid in the blood of young adult humans. Levels in humans decline with age and during certain types of illness or stress. We have found that DHEA(S) can prevent or reduce the neurotoxic actions in the hippocampus of the glutamate agonists N-methyl-d-aspartic acid (NMDA) both in vitro and in vivo or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid in vitro. Pre-treatment with DHEA (10-100 nM for 6-8 h) protected primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity (0.1, 1, 10, and 50 mM). DHEA added either with NMDA (1 mM) or 1 h later had lesser, but still significant, protective actions. DHEAS also reduced NMDA-induced toxicity (1 mM), although the lowest effective dose of DHEAS (100 nM) was higher than that of DHEA (10 nM). DHEA (100 nM) protected cultured neurons against the neurotoxic actions of either AMPA (25 μM) or kainic acid (1 mM) as well. In vivo, s.c. pellets of ...

2In slices, the potencies of the weakly (or non-) transported analogues, N-methyl-D-aspartate (NMDA) and kainate (KA) (EC50 = 40 μM each) were higher than those of the transported amino acids, D- and L-aspartate (EC50 = 250 μM and 300 μM) and D- and L-glutamate (EC50 = 540 μM and 480 μM). Quisqualate (up to 300 μM) failed to increase cyclic GMP levels significantly. The sensitivity of agonist responses to the NMDA receptor antagonist, DL-2-amino-5-phosphonovalerate (APV), was in the order NMDA , L-aspartate , L-glutamate, KA ...

QNZ46 is a NMDA receptor antagonist. QNZ46 inhibits NMDA receptor function in a noncompetitive and voltage-independent manner by an unconventional mechanism that requires binding of glutamate to the GluN2 subunit, but not glycine binding to the GluN1 subunit. QNZ46 could provide an opportunity for the development of pharmacological tools and therapeutic agents that target NMDA receptors at a new site and modulate function by a novel mechanism. NMDA receptors are ionotropic glutamate receptors that mediate excitatory synaptic transmission and have been implicated in several neurological diseases.

Transgenic Huntingtons disease (HD) mice, expressing exon 1 of the human HD gene (lines R6/1 and R6/2), are totally resistant to striatal lesions caused by the NMDA receptor agonist quinolinic acid (QA). Here we show that this resistance develops gradually over time in both R6/1 and R6/2 mice, and that it occurred earlier in R6/2 (CAG-155) than in R6/1 (CAG-115) mice. The development of the resistance coincided with the appearance of nuclear inclusions and with the onset of motor deficits. In the HD mice, hippocampal neurons were also resistant to QA, especially in the CA1 region. Importantly, there was no change in susceptibility to QA in transgenic mice with a normal CAG repeat (CAG-18). R6/1 mice were also resistant to NMDA-, but not to AMPA-induced striatal damage. Interestingly, QA-induced current and calcium influx in striatal R6/2 neurons were not decreased. However, R6/2 neurons had a better capacity to handle cytoplasmic calcium ([Ca2+](c)) overload following OA and could avoid ...

Long-term potentiation of NMDA-receptor-mediated synaptic transmission (NMDAR-LTP) is a little-understood form of plasticity. In the present study, we investigated whether NMDAR-LTP in the dentate gyrus involves recruitment of extrasynaptic NMDARs, because NMDARs are expressed both synaptically and extrasynaptically with evidence for subtype differences at different locations. We show that before induction of NMDAR-LTP, pharmacological inhibition of glutamate transporters resulted in glutamate spillover from the synapse and activation of extrasynaptic NMDARs. After the induction of NMDAR-LTP, such activation of extrasynaptic NMDARs was absent. Activation of extrasynaptic NMDARs after glutamate uptake inhibition also occurred when synaptic NMDARs were inhibited with MK801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate], and this extrasynaptically mediated NMDAR-EPSC was strongly reduced by prior induction of NMDAR-LTP. The extrasynaptic NMDARs were shown to be ...

TY - JOUR. T1 - Hypoxia modulates nitric oxide-induced regulation of NMDA receptor currents and neuronal cell death. AU - Gbadegesin, Muyiwa. AU - Vicini, Stefano. AU - Hewett, Sandra. AU - Wink, David A.. AU - Espey, Michael. AU - Pluta, Ryszard M.. AU - Colton, Carol A.. PY - 1999. Y1 - 1999. N2 - Nitric oxide (NO) released from a new chemical class of donors enhances N-methyl-D-aspartate (NMDA) channel activity. Using whole cell and single- channel patch-clamp techniques, we have shown that (Z)-1-[N(3-ammoniopropyl)- N-(n-propyl)amino]-NO (PAPA-NO) and diethylamine NO, commonly termed NONOates, potentiate the glutamate-mediated response of recombinant rat NMDA receptors(NR1/NR2A) expressed in HEK-293 cells. The overall effect is an increase in both peak and steady-state whole cell currents induced by glutamate. Single-channel studies demonstrate a significant increase in open probability but no change in the mean single-channel open time or mean channel conductance. Reduction in oxygen levels ...

Toxicol Lett. 2011 Sep 10;205(3):336-40. Epub 2011 Jun 24. Chen HH, Lin YR, Chan MH. Source Institute of Pharmacology and Toxicology, Tzu Chi University, 701, Sec. 3, Chung Yang Rd., Hualien 97004, Taiwan. Abstract Toluene, an industrial organic solvent, is voluntarily inhaled as drug of abuse. Because inhibition of N-methyl-d-aspartate (NMDA) receptors is one of…

TY - JOUR. T1 - Neuronal and glial localization of NMDA receptors in the cerebral cortex. AU - Conti, Fiorenzo. AU - Minelli, Andrea. AU - DeBiasi, Silvia. AU - Melone, Marcello. PY - 1997/2. Y1 - 1997/2. N2 - The crucial role of glutamate receptors of the N-methyl-D-aspartate (NMDA) type in many fundamental cortical functions has been firmly established, as has its involvement in several neuropsychiatric diseases, but until recently, very little was known of the anatomical localization of NMDA receptors in the cerebral cortex of mammals. The recent application of molecular biological techniques to the study of NMDA receptors has allowed the production of specific tools, the use of which has much increased our understanding of the localization of NMDA receptors in the cerebral cortex. In particular, immunocytochemical studies on the distribution of cortical NMDA receptors have: 1. Demonstrated the preferential localization of NMDA receptors in dendritic spines, in line with previous work; 2. ...

Polyamine potentiation and inhibition of NMDA-mediated increases of intracellular free Ca2+ in cultured chick cortical neurons. Eur J Pharmacol. 1994 Jan 15; 266(2):107-15 ...

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D-Cycloserine, a partial agonist of the glycine recognition site of the N-methyl- D-aspartate ( NM DA) receptor, may serve as a probe for human cerebral NM DA receptor function. Since NM DA receptors

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GRIN2A - GRIN2A (untagged)-Human glutamate receptor, ionotropic, N-methyl D-aspartate 2A (GRIN2A), transcript variant 1 available for purchase from OriGene - Your Gene Company.

Biology of the NMDA Receptor - free book at E-Books Directory. You can download the book or read it online. It is made freely available by its author and publisher.

Sigma-1 (σ1) receptor has been identified as a chaperone protein that interacts with other proteins, such as N-methyl-D-aspartate… Expand ...

Its been a heck of a week, friends. Friday was a trip to the pain management clinic, which -- per usual -- was wholeheartedly depressing. I find that I feel even worse whenever I come out of those appointments because I realize how useless they are. Pain management clinics, that is. Massachusetts as a whole is…

Looking for online definition of N-methyl D-aspartate receptor subtype 2C in the Medical Dictionary? N-methyl D-aspartate receptor subtype 2C explanation free. What is N-methyl D-aspartate receptor subtype 2C? Meaning of N-methyl D-aspartate receptor subtype 2C medical term. What does N-methyl D-aspartate receptor subtype 2C mean?

TY - JOUR. T1 - Endogenous D-serine contributes to NMDA-receptor-mediated light-evoked responses in the vertebrate retina. AU - Gustafson, Eric C.. AU - Stevens, Eric R.. AU - Wolosker, Herman. AU - Miller, Robert F.. N1 - Copyright: Copyright 2009 Elsevier B.V., All rights reserved.. PY - 2007/7. Y1 - 2007/7. N2 - We have combined electrophysiology and chemical separation and measurement techniques with capillary electrophoresis (CE) to evaluate the role of endogenous D-serine as an NMDA receptor (NMDAR) coagonist in the salamander retina. Electrophysiological experiments were carried out using whole cell recordings from retinal ganglion cells and extracellular recordings of the proximal negative response (PNR), while bath applying two D-serine degrading enzymes, including Damino acid oxidase (DAAO) and D-serine deaminase (DsdA). The addition of either enzyme resulted in a significant and rapid decline in the light-evoked responses observed in ganglion cell and PNR recordings. The addition of ...

TY - JOUR. T1 - Pathologically activated neuroprotection via uncompetitive blockade of N-methyl-D-aspartate receptors with fast off-rate by novel multifunctional dimer bis(propyl)-cognitin. AU - Luo, Jialie. AU - Li, Wenming. AU - Zhao, Yuming. AU - Fu, Hongjun. AU - Ma, Dik Lung. AU - Tang, Jing. AU - Li, Chaoying. AU - Peoples, Robert W.. AU - Li, Fushun. AU - Wang, Qinwen. AU - Huang, Pingbo. AU - Xia, Jun. AU - Pang, Yuanping. AU - Han, Yifan. PY - 2010/6/25. Y1 - 2010/6/25. N2 - Uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists with fast off-rate (UFO) may represent promising drug candidates for various neurodegenerative disorders. In this study, we report that bis(propyl)-cognitin, a novel dimeric acetylcholinesterase inhibitor and γ-aminobutyric acid subtype A receptor antagonist, is such an antagonist of NMDA receptors. In cultured rat hippocampal neurons, we demonstrated that bis-(propyl)-cognitin voltage-dependently, selectively, and moderately inhibited NMDA-activated ...

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TITLE AMPA and NMDA receptor with presynaptic short-term plasticity COMMENT AMPA and NMDA receptor conductance using a dual-exponential profile presynaptic short-term plasticity based on Fuhrmann et al. 2002 Implemented by Srikanth Ramaswamy, Blue Brain Project, July 2009 Etay: changed weight to be equal for NMDA and AMPA, gmax accessible in Neuron ENDCOMMENT NEURON { POINT_PROCESS ProbAMPA RANGE tau_r_AMPA, tau_d_AMPA, tau_r_NMDA, tau_d_NMDA RANGE Use, u, Dep, Fac, u0, weight_NMDA RANGE i, i_AMPA, i_NMDA, g_AMPA, g_NMDA, e, gmax, mgVoltageCoeff NONSPECIFIC_CURRENT i POINTER rng } PARAMETER { tau_r_AMPA = 0.2 (ms) : dual-exponential conductance profile tau_d_AMPA = 1.7 (ms) : IMPORTANT: tau_r , tau_d tau_r_NMDA = 0.00000001 (ms) : dual-exponential conductance profile tau_d_NMDA = 0.00000002 (ms) : IMPORTANT: tau_r , tau_d Use = 1.0 (1) : Utilization of synaptic efficacy (just initial values! Use, Dep and Fac are overwritten by BlueBuilder assigned values) Dep = 100 (ms) : relaxation time ...

A series of 2-substituted 3,4-dihydro-2H-1,2-benzothiazine-3-carboxylic acid 1,1-dioxides were synthesized and evaluated for their affinity to the glycine binding site of the N-methyl-d-aspartate (NMDA) receptor. The binding affinity was determined by the displacement of radioligand [(3)H]MDL-105,519 from rat cortical membrane preparations. The most attractive structures in the search for prospective NMDA receptor ligands were identified to be 2-arylcarbonylmethyl substituted 3,4-dihydro-2H-1,2-benzothiazine-3-carboxylic acid 1,1-dioxides. It has been demonstrated for the first time that the replacement of NH group in the ligand by sp(3) CH2 is tolerated. This finding may pave the way for previously unexplored approaches for designing new ligands of the NMDA receptor.

AbstractIn the present study, a twenty-mer antisense oligonucleotide specific for N-methyl-D-aspartate receptor one (ANR1) was applied to striatal neurons in primary cell culture. The ANR1 was found to be specific and nontoxic. Significant reductions in expression of NR1 mRNA and proteins were resulted after a single dose of ANR1 transcripts. Interestingly, there were reductions in total NR1 proteins but two phosphorylated forms of NR1 proteins at serine 896 and 897 residues were not reduced. There was also no change in the pattern of distribution of NR1 immunoreactivity in the striatal neurons. In addition, significant reductions of NMDA-mediated peak inward current were found after application of a higher concentration of ANR1 (20-100 mu M) by patch clamp recordings. The present results indicate that ANR1 is a useful agent in reducing NMIDA receptor functions. The present data thus provide detailed cellular and molecular mechanisms to explain our previous findings of amelioration of motor ...

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Electrical activation of hippocampal neurons can cause calcium influx through different entry sites which may specify nuclear signalling and induction of gene transcription and downstream physiological outputs. Genomic responses initiated by NMDA receptors (NMDARs) are critically dependent on whethe …

Looking for online definition of excitotoxic in the Medical Dictionary? excitotoxic explanation free. What is excitotoxic? Meaning of excitotoxic medical term. What does excitotoxic mean?

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Sigma-Aldrich offers abstracts and full-text articles by [Fernando A Giuliani, Roberto Yunes, Claudia E Mohn, Myriam Laconi, Valeria Rettori, Ricardo Cabrera].

   Forgive me if some of this is repetitive, much of this has been posted on our Ketamine thread, but I felt like it deserved a thread of its own. Ever since I ended up in the ER with a cluster and they gave me I.V. magnesium I have been interested in glutamate toxicity in the brain. I could...

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Olneys lesions Olneys lesions, also known as NMDA receptor antagonist neurotoxicity (NAN), are a form of brain damage caused by high doses of dissociative

As I said, oxytosis, otherwise known as excitotoxicity or glutamate toxicity Hi, justy. I think that what you are experiencing are symptoms of...

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