INT135113

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Context Info
Confidence 0.73
First Reported 2006
Last Reported 2011
Negated 1
Speculated 0
Reported most in Body
Documents 18
Total Number 18
Disease Relevance 3.73
Pain Relevance 7.69

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

transport (Grin1) plasma membrane (Grin1) enzyme binding (Grin1)
cytoplasm (Grin1)
Anatomy Link Frequency
CeA 3
pyramidal neurons 1
neurons 1
brain 1
cortex 1
Grin1 (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 33 99.68 Very High Very High Very High
opioid receptor 87 99.56 Very High Very High Very High
nMDA receptor 98 99.48 Very High Very High Very High
Morphine 92 98.82 Very High Very High Very High
Antinociceptive 3 98.36 Very High Very High Very High
Pyramidal cell 88 98.16 Very High Very High Very High
imagery 77 97.82 Very High Very High Very High
Potency 2 97.40 Very High Very High Very High
Opioid 41 97.04 Very High Very High Very High
qutenza 1 96.16 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 122 99.96 Very High Very High Very High
Reperfusion Injury 1 98.60 Very High Very High Very High
Nociception 19 97.44 Very High Very High Very High
Urological Neuroanatomy 95 93.36 High High
Opiate Addiction 18 93.36 High High
Pain 24 89.76 High High
Congenital Anomalies 32 88.24 High High
INFLAMMATION 29 86.88 High High
Inflammatory Pain 13 83.12 Quite High
Injury 20 68.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Morphine pretreatment significantly inhibited nPKCepsilon membrane translocation and phosphorylation of NR1 subunits of NMDA receptors during reperfusion injury.
Localization (translocation) of NR1 associated with reperfusion injury, nmda receptor and morphine
1) Confidence 0.73 Published 2006 Journal J Neurosurg Anesthesiol Section Abstract Doc Link 16628065 Disease Relevance 0.17 Pain Relevance 1.00
To overcome these shortcomings, high-resolution imaging and molecular pharmacology were used to (1) Identify the ultrastructural localization of the essential NMDA-NR1 receptor (NR1) subunit and its relationship to the mu-opioid receptor (microOR), the major cellular target of abused opioids like morphine, in the CeA and (2) Determine the effect of CeA NR1 deletion on the physical, and particularly, psychological aspects of opioid dependence.
Localization (relationship) of NR1 in CeA associated with addiction, opioid receptor, amygdala, opioid, imagery and morphine
2) Confidence 0.70 Published 2010 Journal Vitam. Horm. Section Abstract Doc Link 20472137 Disease Relevance 0.26 Pain Relevance 1.29
To overcome these shortcomings, high-resolution imaging and molecular pharmacology were used to (1) Identify the ultrastructural localization of the essential NMDA-NR1 receptor (NR1) subunit and its relationship to the mu-opioid receptor (microOR), the major cellular target of abused opioids like morphine, in the CeA and (2) Determine the effect of CeA NR1 deletion on the physical, and particularly, psychological aspects of opioid dependence.
Localization (relationship) of NR1 in CeA associated with addiction, opioid receptor, amygdala, opioid, imagery and morphine
3) Confidence 0.70 Published 2010 Journal Vitam. Horm. Section Abstract Doc Link 20472137 Disease Relevance 0.26 Pain Relevance 1.28
Mice with deletion of NR1 in the CeA showed no obvious impairments in sensory, motor, or nociceptive function.
Localization (deletion) of NR1 in CeA associated with nociception and amygdala
4) Confidence 0.70 Published 2010 Journal Vitam. Horm. Section Abstract Doc Link 20472137 Disease Relevance 0.53 Pain Relevance 1.47
Thus, the localized deficit of NR1 mRNA in transduced cells is not due to some spurious effect of lentivector transduction, but to KO of the fNR1 gene.
Localization (localized) of NR1 mRNA associated with targeted disruption
5) Confidence 0.60 Published 2007 Journal Frontiers in Integrative Neuroscience Section Body Doc Link PMC2526007 Disease Relevance 0.31 Pain Relevance 0.04
In this report, we demonstrate that a mammalian codon optimized Cre (Shimshek et al., 2002) expressed from a lentivector (Naldini et al., 1996) in fNR1 mice can transduce cortical cells in a layer- and column-specific manner (Aronoff and Petersen, 2006; Dittgen et al., 2004), generating highly localized NR1 KO and concomitant loss of NMDAR function in pyramidal neurons.
Localization (localized) of NR1 in pyramidal neurons associated with targeted disruption and pyramidal cell
6) Confidence 0.60 Published 2007 Journal Frontiers in Integrative Neuroscience Section Body Doc Link PMC2526007 Disease Relevance 0.10 Pain Relevance 0.12
The absence of Neto1 had no effect on the overall abundance of NR1, NR2A, NR2B, PSD-95, GluR2, VAMP2, or GABAAR1 proteins (Figure 6L) in whole brain extracts, or of NR1, NR2A, NR2B, or PSD-95 in crude synaptosomes (Figure 6M).
Localization (abundance) of NR1 in brain
7) Confidence 0.57 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.17 Pain Relevance 0.05
Moreover, the amount of NR2A, NR2B, and PSD-95 that co-immunoprecipitated with NR1 from crude synaptosomes was normal in Neto1-null mice, indicating that the lack of Neto1 did not alter the overall abundance of the NMDAR:PSD-95 holocomplex (Figure 6N).


Localization (immunoprecipitated) of NR1
8) Confidence 0.57 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.15 Pain Relevance 0.07
20HA co-immunoprecipitated with both NR2A (Figure 5A, lanes 1 and 2, and Figure 5C, lane 4) and NR2B (Figure 5B, lanes 1 and 2, and Figure 5C, lane 5) expressed in the absence of NR1 and PSD-95.
Neg (absence) Localization (absence) of NR1
9) Confidence 0.57 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0
Moreover, the amount of NR2A, NR2B, and PSD-95 that co-immunoprecipitated with NR1 from crude synaptosomes was normal in Neto1-null mice, indicating that the lack of Neto1 did not alter the overall abundance of the NMDAR:PSD-95 holocomplex (Figure 6N).


Localization (abundance) of NMDAR
10) Confidence 0.57 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.14 Pain Relevance 0.08
Cryosections from fNR1 mice, which had been injected with lentivector encoding GFP and Cre, were hybridized to an antisense NR1 cDNA probe to assay NR1 mRNA abundance (Figure 6B).
Localization (abundance) of NR1
11) Confidence 0.52 Published 2007 Journal Frontiers in Integrative Neuroscience Section Body Doc Link PMC2526007 Disease Relevance 0.21 Pain Relevance 0
Cryosections from fNR1 mice, which had been injected with lentivector encoding GFP and Cre, were hybridized to an antisense NR1 cDNA probe to assay NR1 mRNA abundance (Figure 6B).
Localization (abundance) of NR1 mRNA
12) Confidence 0.52 Published 2007 Journal Frontiers in Integrative Neuroscience Section Body Doc Link PMC2526007 Disease Relevance 0.21 Pain Relevance 0
Because basal synaptic transmission (Figure 7) and AMPAR-EPSCs (Figure S5) in Neto1-null neurons were not different from wild-type, we interpret the decrease in NMDAR:AMPAR EPSC ratio as indicating that synaptic NMDAR currents were reduced in Neto1-null neurons.
Localization (decrease) of NMDAR in neurons
13) Confidence 0.49 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.07 Pain Relevance 0.10
We do not exclude the possibility that NMDAR NR1 subunit is altered in our experiment condition.
Localization (altered) of NMDAR NR1 subunit
14) Confidence 0.45 Published 2009 Journal Mol Pain Section Body Doc Link PMC2803476 Disease Relevance 1.02 Pain Relevance 1.03
This characteristic contributes to the long-term NMDAR-mediated desensitization of MORs that is observed even after the antinociceptive effects of a desensitizing dose of morphine have disappeared.
Localization (desensitization) of NMDAR associated with antinociceptive and morphine
15) Confidence 0.41 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0.11 Pain Relevance 1.07
After blocking nonspecific protein interactions with 10% albumin in Tris-buffered saline (TBS), the nitrocellulose papers were incubated for 2 hr at room temperature with the primary antibodies: NR1 (1:1000; Pharmingen, San Diego, CA, USA), NR2A (1:1000; Zymed, San Francisco, CA, USA), NR2B (1:1000; Zymed), GluR1 (1:1500; Chemicon, Temecula, CA, USA), PSD-95 (1:2000; Affinity BioReagents, Golden, CO, USA), SAP97 (1:1000; StressGen, San Diego, CA, USA), Ca2+/calmodulin-dependent protein kinase II (?
Localization (1:1000) of NR1
16) Confidence 0.16 Published 2007 Journal Environ Health Perspect Section Body Doc Link PMC1892123 Disease Relevance 0 Pain Relevance 0
Interestingly, MHCI-HC protein detected in this study also localized to NMDAR1-positive neurons in the cortex of enucleated animals (Additional file 7), which is also indicative of MHCI association with neuronal activity [61,70].
Localization (localized) of NMDAR1 in cortex
17) Confidence 0.15 Published 2011 Journal Behav Brain Funct Section Body Doc Link PMC3023691 Disease Relevance 0 Pain Relevance 0
Our results suggest that Dimebon does not display selectivity for NR2B subtype of NMDAR, as both WT and YAC128 MSN currents were inhibited with similar potency (Fig 3B).
Localization (subtype) of NMDAR associated with potency
18) Confidence 0.10 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2577671 Disease Relevance 0 Pain Relevance 0.09

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