INT110705

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Context Info
Confidence 0.69
First Reported 2003
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 11
Total Number 16
Disease Relevance 4.70
Pain Relevance 7.33

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
brain 8
spinal 2
spines 2
synapses 2
hippocampus 2
Grin1 (Mus musculus)
Pain Link Frequency Relevance Heat
Central grey 77 100.00 Very High Very High Very High
nMDA receptor 49 100.00 Very High Very High Very High
Glutamate 17 100.00 Very High Very High Very High
depression 124 99.82 Very High Very High Very High
Physical dependence 12 99.76 Very High Very High Very High
central sensitization 4 99.76 Very High Very High Very High
dopamine receptor 1 99.56 Very High Very High Very High
Hippocampus 111 99.38 Very High Very High Very High
Pain 30 99.28 Very High Very High Very High
Morphine 4 98.96 Very High Very High Very High
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 77 100.00 Very High Very High Very High
Depression 124 99.82 Very High Very High Very High
Drug Dependence 12 99.76 Very High Very High Very High
Pain 31 99.28 Very High Very High Very High
Hyperalgesia 11 97.04 Very High Very High Very High
Neuropathic Pain 6 96.36 Very High Very High Very High
INFLAMMATION 23 91.28 High High
Nociception 15 90.84 High High
Targeted Disruption 29 88.96 High High
Injury 17 79.68 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
At the molecular level, maintenance of central sensitization is largely dependent on the N-methyl-D-aspartate receptor (NMDAR) activation.
Positive_regulation (dependent) of Positive_regulation (activation) of N-methyl-D-aspartate receptor associated with central sensitization and nmda receptor
1) Confidence 0.69 Published 2003 Journal Neurosci. Res. Section Abstract Doc Link 12767483 Disease Relevance 0.56 Pain Relevance 0.68
At the molecular level, maintenance of central sensitization is largely dependent on the N-methyl-D-aspartate receptor (NMDAR) activation.
Positive_regulation (dependent) of Positive_regulation (activation) of NMDAR associated with central sensitization and nmda receptor
2) Confidence 0.50 Published 2003 Journal Neurosci. Res. Section Abstract Doc Link 12767483 Disease Relevance 0.56 Pain Relevance 0.68
In some experiments show that activation of NMDARs in the PAG causes an inhibition of pain response [21,43,44], while others show that NMDARs may play a critical role in induction of spinal hyperalgesia after prolonged noxious stimulation [1,2,20].
Positive_regulation (causes) of Positive_regulation (activation) of NMDAR in spinal associated with pain, hyperalgesia and central grey
3) Confidence 0.49 Published 2009 Journal Mol Pain Section Body Doc Link PMC2803476 Disease Relevance 1.25 Pain Relevance 0.67
The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p-CaMKII) protein, c-fos mRNA, c-Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone-precipitated withdrawal.
Positive_regulation (observed) of Positive_regulation (levels) of NR1 in brain associated with glutamate, nmda receptor, narcan and withdrawal
4) Confidence 0.39 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15464026 Disease Relevance 0.36 Pain Relevance 0.94
The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p-CaMKII) protein, c-fos mRNA, c-Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone-precipitated withdrawal.
Positive_regulation (increased) of Positive_regulation (levels) of NR1 in brain associated with glutamate, nmda receptor, narcan and withdrawal
5) Confidence 0.39 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15464026 Disease Relevance 0.24 Pain Relevance 0.70
The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p-CaMKII) protein, c-fos mRNA, c-Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone-precipitated withdrawal.
Positive_regulation (increased) of Positive_regulation (levels) of receptor zeta subunit in brain associated with glutamate, nmda receptor, narcan and withdrawal
6) Confidence 0.34 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15464026 Disease Relevance 0.24 Pain Relevance 0.70
The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p-CaMKII) protein, c-fos mRNA, c-Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone-precipitated withdrawal.
Positive_regulation (observed) of Positive_regulation (levels) of receptor zeta subunit in brain associated with glutamate, nmda receptor, narcan and withdrawal
7) Confidence 0.34 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15464026 Disease Relevance 0.36 Pain Relevance 0.94
Taken together, these data indicate that NMDAR activation is enhanced by mAChR activation under conditions where Mg2+ block of NMDARs is present (Figure 4C; ?
Positive_regulation (enhanced) of Positive_regulation (activation) of NMDAR
8) Confidence 0.33 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.14
Taken together, these data indicate that NMDAR activation is enhanced by mAChR activation under conditions where Mg2+ block of NMDARs is present (Figure 4C; ?
Positive_regulation (by) of Positive_regulation (activation) of NMDAR
9) Confidence 0.33 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.14
While this may indeed be the case, our data indicate that KCNQ channels do not mediate the facilitation of NMDAR function induced by M1 receptor activation since blockade of KCNQ channels with XE-991 did not prevent the actions of M1 receptor activation on NMDAR function (Figure 6).
Neg (not) Positive_regulation (mediate) of Positive_regulation (induced) of NMDAR
10) Confidence 0.33 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0.06 Pain Relevance 0.10
The depolarization and increase in input resistance caused by the activation of M1 receptors could also enhance NMDAR activation during synaptic transmission and in particular during TBP.
Positive_regulation (enhance) of Positive_regulation (activation) of NMDAR
11) Confidence 0.30 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.07
Although KCNQ channels are thought to be preferentially targeted to the somatic membrane and are not present on dendritic spines, their blockade may still increase NMDAR activation as a result of cellular membrane depolarization and increase in input resistance (Hu et al., 2007; Yue and Yaari, 2004).
Spec (may) Positive_regulation (increase) of Positive_regulation (activation) of NMDAR in spines
12) Confidence 0.30 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0.07 Pain Relevance 0.05
This suggests that enhancement of NMDAR activation by mAChRs could be the mechanism for the facilitation of LTP by 77-LH-28-1.
Positive_regulation (enhancement) of Positive_regulation (activation) of NMDAR associated with long-term potentiation
13) Confidence 0.30 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.26
Homosynaptic LTP at layer 4 to 2/3 synapses as well as at layer 2/3 to 5 synapses requires NMDAR activation (Kirkwood et al. 1993; Wang & Daw 2003), whereas synaptic scaling in culture does not (Turrigiano et al. 1998; Turrigiano & Nelson 2004).
Positive_regulation (requires) of Positive_regulation (activation) of NMDAR in synapses associated with long-term potentiation
14) Confidence 0.27 Published 2008 Journal Philosophical Transactions of the Royal Society B: Biological Sciences Section Body Doc Link PMC2674473 Disease Relevance 0.11 Pain Relevance 0.22
Behavioral analyses found that GluR2-cKO mice were impaired on multiple hippocampus-dependent learning tasks that required NMDAR activation.
Positive_regulation (required) of Positive_regulation (activation) of NMDAR in hippocampus associated with hippocampus
15) Confidence 0.23 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2947514 Disease Relevance 0.09 Pain Relevance 0.28
In the PrPFC, eCB-LTD did not require the activation of NMDAR, D1 or D2 dopamine receptors, as demonstrated by the lack of effects of a cocktail of antagonist of these receptors (Fig 5A).
Neg (not) Positive_regulation (require) of Positive_regulation (activation) of NMDAR associated with depression, antagonist and dopamine receptor
16) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1933592 Disease Relevance 0.80 Pain Relevance 0.75

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