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83 results for “NMDA”
Dataset for article: Pro-cognitive effects of dual tacrine derivatives acting as cholinesterase inhibitors and NMDA receptor antagonists
<p>Figure 1. Chemical structures of tacrine (<strong>a</strong>) and its derivatives created by introducing substituents on the aromatic core and/or altering the size of the cycloalkyl moiety attached to the aromatic region: 7-MEOTA (<strong>b</strong>), K1578 (7-chloro-1<em>H</em>,2<em>H</em>,3<em>H</em>-cyclopenta[<em>b</em>]quinolin-9-amine; <strong>c</strong>), K1592 (1-chloro-6<em>H</em>,7<em>H</em>,8<em>H</em>,9<em>H</em>,10<em>H</em>-cyclohepta[<em>b</em>]quinolin-11-amine; <strong>d</strong>), K1594 (6-methyl-1,2,3,4-tetrahydroacridin-9-amine; <strong>e</strong>), and K1599 (7-methoxy-1<em>H</em>,2<em>H</em>,3<em>H</em>-cyclopenta[<em>b</em>]quinolin-9-amine; <strong>f</strong>). Compounds in this study were used in the form of hydrochloride salts.</p> <p>Figure_2_values. Test results. Morris water maze: scopolamine-induced model of cognitive deficit in the acquisition and reversal phases. The graphs show the effects of K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on escape latency during the acquisition phase, where none of the compounds ameliorated the deficit of spatial learning. The remaining graphs display the effects of K1578 (<strong>e</strong>), K1592 (<strong>f</strong>), K1594 (<strong>g</strong>), and K1599 (<strong>h</strong>) in the reversal phase, where K1578 (1 mg/kg) and K1599 (at both doses), and marginally K1592 (1 mg/kg; see in the text), mitigated the scopolamine-induced deficit of reversal learning. VEH – vehicle, the numbers in brackets denote the dose applied (mg/kg). Data are presented as the mean + SEM, * vs. VEH, * p < 0.05, ** p < 0.01, *** p < 0.001. <em>n</em> = 6–9 animals per group. Statistical significance was determined using two-way repeated measures ANOVA (a–d) or ANOVA (e, f, h) followed by Dunnett’s multiple comparisons tests.</p> <p>Figure-3_values. Test results. Morris water maze: MK-801-induced model of cognitive deficit in the acquisition phase. The graphs illustrate the effects of the compounds K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on escape latency. Only K1599 (1 mg/kg) ameliorated the MK-801-induced deficit of spatial learning. VEH – vehicle, the numbers in brackets denote the dose (mg/kg). Data are presented as the mean + SEM, * vs. VEH, * p < 0.05, ** p < 0.01. <em>n</em> = 5–7 animals per group. Statistical significance was determined using two-way repeated measures ANOVA followed by Dunnett’s multiple comparisons tests.</p> <p>Figure_4_values. Open field test. The results demonstrate the effects of K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on the distance moved by intact and MK-801-treated animals. VEH – vehicle, the numbers in brackets denote the dose (mg/kg). Data are presented as the mean + SEM, * vs. VEH group of the corresponding phenotype, * p < 0.05, ** p < 0.01, **** p < 0.0001. <em>n</em> = 6–14 animals per group. A significant effect of both factors (treatment and phenotype) was determined using two-way ANOVA, followed by Dunnett’s multiple comparisons tests.</p> <p>Figure-5_values. Acetylcholinesterase activity. The results document the effect of the compounds (1 mg/kg ip) on AChE activity in the hippocampus (<strong>a</strong>), prefrontal cortex (<strong>b</strong>), striatum (<strong>c</strong>), and whole brain sample (<strong>d</strong>). K1578 and K1599 decreased AChE activity in the striatum. VEH – vehicle. Data are presented as the median with minimum to maximum range, * vs. VEH, *** p < 0.001, **** p < 0.0001. VEH samples AChE enzyme activities reached the following absolute values (a) 15.19 ± 3.09 U/mg protein, (b) 9.810 ± 1.54 U/mg protein, (c) 26.05 ± 3.27 U/mg protein, and (d) 27.38 ± 3.36 U/mg protein. Significance was determined by ANOVA (graphs c, d), followed by Dunnett’s multiple comparisons tests.</p> <p>Figure_6_values. Electrophysiology: Inhibition of GluN1/GluN2A receptors by K1599. Representative whole-cell patch-clamp recordings measured from HEK293 cells expressing the GluN1/GluN2A receptors held at a membrane voltage of −80 mV and +60 mV; 30 μM K1599 was applied as indicated. Results summarizing the relative inhibition induced by 30 µM K1599, measured at the indicated membrane potentials. <em>n</em> ≥ 5 cells per each condition.</p> <p>Table_1. The rats were pseudo-randomly assigned to one of the 18 treatment groups listed in. Each group received two injections: one containing the study compound and another containing either MK-801 or scopolamine, as indicated by the group name. The vehicle group (VEH) received the DMSO vehicle (2.5 mL/kg) and saline. The “scopolamine” and “MK-801” groups received scopolamine or MK-801, respectively, along with the DMSO vehicle (2.5 mL/kg).</p> <p>Table 2. Treatment groups and <em>n</em> in biochemical experiments - AChE activity assay.</p>
NMDA receptors in visual cortex are necessary for normal visuomotor integration and skill learning
<p>Raw data and Matlab code to generate the figures of the publication "NMDA receptors in visual cortex are necessary for normal visuomotor integration and skill learning" <a href="https://doi.org/10.7554/eLife.71476">https://doi.org/10.7554/eLife.71476</a>. Run generate_NKO_figures.m to produce all figures in the publication. </p>
Dataset for article: Dizocilpine derivatives as neuroprotective NMDA receptor antagonists without psychomimetic side effects
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MRI NMDA-lesioned
<p>NMDA ReRh-lesioned rats, MRI images, NeuN immunostaining pictures, cresyl violet staining pictures, groups</p>
Dataset for article: Potent and reversible open-channel blocker of NMDA receptor derived from dizocilpine with enhanced membrane-to-channel inhibition
<div>This version shows the correct number of n for Figure 6.</div> <div> </div>
Data for: Excitatory and inhibitory D-serine binding to the NMDA receptor
<p>N-methyl-D-aspartate receptors (NMDARs) uniquely require binding of two different neurotransmitter agonists for synaptic transmission. D-serine and glycine bind to one subunit, GluN1, while glutamate binds to the other, GluN2. These agonists bind to the receptor's bi-lobed ligand-binding domains (LBDs), which close around the agonist during receptor activation. To better understand the unexplored mechanisms by which D-serine contributes to receptor activation, we performed multi-microsecond molecular dynamics simulations of the GluN1/GluN2A LBD dimer with free D-serine and glutamate agonists. Surprisingly, we observed D-serine binding to both GluN1 and GluN2A LBDs, suggesting that D-serine competes with glutamate for binding to GluN2A. This mechanism is confirmed by our electrophysiology experiments, which show that D-serine is indeed inhibitory at high concentrations. Although free energy calculations indicate that D-serine stabilizes the closed GluN2A LBD, its inhibitory behavior suggests that it either does not remain bound long enough or does not generate sufficient force for ion channel gating. We developed a workflow using pathway similarity analysis to identify groups of residues working together to promote binding. These conformation-dependent pathways were not significantly impacted by the presence of N-linked glycans, which act primarily by interacting with the LBD bottom lobe to stabilize the closed LBD.</p>
The Impact of Pharmacological and Electric Modulation of NMDA Pathway on the Cognitive Flexibility and Volitional Movement Preparation in Patients With Parkinson's Disease
ClinicalTrials.gov study NCT01785628. IPD Sharing: Not stated. Countries: 1. Publications: 1.
NMDA Receptors in Motor Learning in Humans
ClinicalTrials.gov study NCT02082912. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Neocortical Layer-5 tLTD Relies on Non-Ionotropic Presynaptic NMDA Receptor Signaling
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Data for: Excitatory and inhibitory D-serine binding to the NMDA receptor
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NMDA receptors involvement in memory and prediction
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Data from: A circuit mechanism for decision making biases and NMDA receptor hypofunction
<table> <tbody> <tr> <td>Decision-making biases can be features of normal behaviour, or deficits underlying neuropsychiatric symptoms. We used behavioural psychophysics, spiking-circuit modelling and pharmacological manipulations to explore decision-making biases during evidence integration. Monkeys showed a pro-variance bias (PVB): a preference to choose options with more variable evidence. The PVB was also present in a spiking circuit model, revealing a potential neural mechanism for this behaviour. To model possible effects of NMDA receptor (NMDA-R) antagonism on this behaviour, we simulated the effects of NMDA-R hypofunction onto either excitatory or inhibitory neurons in the model. These were then tested experimentally using the NMDA-R antagonist ketamine, a pharmacological model of schizophrenia. Ketamine yielded an increase in subjects' PVB consistent with lowered cortical excitation/inhibition balance from NMDA-R hypofunction predominantly onto excitatory neurons. These results provide a circuit-level mechanism that bridges across explanatory scales, from the synaptic to the behavioural, in neuropsychiatric disorders where decision-making biases are prominent.</td> </tr> <tr> </tr> </tbody> </table>
NMDA Enhancer for the Treatment of Mild Alzheimer's Disease
ClinicalTrials.gov study NCT03752463. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Antioxidant and NMDA Receptor Blocker Wins Anoxic Brain Damage of KorEa OHCA Patients
ClinicalTrials.gov study NCT03651557. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
NMDA Modulation in Major Depressive Disorder in Late- Life
ClinicalTrials.gov study NCT03414931. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Transcranial Direct Current Stimulation on Cortical Plasticity in Patients With Anti-NMDA Receptor Encephalitis
ClinicalTrials.gov study NCT01865578. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Mineralocorticoid Receptor, NMDA Receptor and Cognitive Function in Depression
ClinicalTrials.gov study NCT03062150. IPD Sharing: NO. Countries: 1. Publications: 4.
Effect of N-methyl D-aspartate (NMDA) Receptor Antagonist Dextromethorphan on Opiods Analgesia and Tolerance in Pediatric Intensive Care Unit Patients
ClinicalTrials.gov study NCT01553435. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Augmenting Exposure Therapy With an N-Methyl-D-Aspartate (NMDA) Agonist for Panic Disorder
ClinicalTrials.gov study NCT00131339. IPD Sharing: Not stated. Countries: 1. Publications: 1.
NMDA Receptor Modulation for Hyperarousal in PTSD
ClinicalTrials.gov study NCT03166501. IPD Sharing: NO. Countries: 1. Publications: 5.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.