INT52194

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Context Info
Confidence 0.69
First Reported 1993
Last Reported 2011
Negated 2
Speculated 5
Reported most in Body
Documents 83
Total Number 88
Disease Relevance 25.09
Pain Relevance 34.76

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
hippocampus 9
neurons 6
neuronal 4
spinal cord 3
synapses 3
Grin1 (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 1615 100.00 Very High Very High Very High
nMDA receptor 303 100.00 Very High Very High Very High
Glutamate 300 100.00 Very High Very High Very High
Spinal cord 86 100.00 Very High Very High Very High
Glutamate receptor 62 100.00 Very High Very High Very High
Dorsal horn 57 100.00 Very High Very High Very High
Hippocampus 885 99.90 Very High Very High Very High
central sensitization 26 99.80 Very High Very High Very High
tetrodotoxin 82 99.76 Very High Very High Very High
Central grey 169 99.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 900 99.96 Very High Very High Very High
Urological Neuroanatomy 324 99.64 Very High Very High Very High
Depression 349 99.58 Very High Very High Very High
Cancer 92 99.54 Very High Very High Very High
Pain 430 99.46 Very High Very High Very High
Drug Dependence 8 99.36 Very High Very High Very High
Hyperalgesia 106 98.80 Very High Very High Very High
Convulsion 534 98.08 Very High Very High Very High
Nociception 135 97.92 Very High Very High Very High
Anxiety Disorder 367 97.88 Very High Very High Very 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 (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 (activation) of NMDAR associated with central sensitization and nmda receptor
2) Confidence 0.69 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 (activation) of NMDAR in spinal associated with pain, hyperalgesia and central grey
3) Confidence 0.67 Published 2009 Journal Mol Pain Section Body Doc Link PMC2803476 Disease Relevance 1.24 Pain Relevance 0.67
The notion of enhanced NMDAR activity in PrP-null mouse neurons is consistent with the enhanced NMDA toxicity observed in our in vitro and in vivo studies and indicates that PrPC provides a degree of neuroprotection from glutamate toxicity.
Positive_regulation (enhanced) of NMDAR in neurons associated with toxicity and glutamate
4) Confidence 0.59 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2364707 Disease Relevance 0.26 Pain Relevance 0.08
Our findings showing increased NMDAR activity in null mice would be consistent with such a mechanism.
Positive_regulation (increased) of NMDAR
5) Confidence 0.59 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2364707 Disease Relevance 0.70 Pain Relevance 0.11
This type of depletion of normal PrPC levels may well mimic some aspects of the phenotype of PrP knockout (such as enhanced NMDAR activity).
Positive_regulation (enhanced) of NMDAR associated with targeted disruption
6) Confidence 0.59 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2364707 Disease Relevance 0.89 Pain Relevance 0.06
Basal synaptic transmission is principally mediated by AMPARs, which are rapidly activated by glutamate, while the more slowly activated NMDAR primarily mediates various forms of synaptic plasticity.
Positive_regulation (activated) of NMDAR associated with glutamate
7) Confidence 0.53 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0.22
We considered that the deficits in LTP and learning might be restored by enhancing the residual NMDAR function in Neto1-null mice.
Positive_regulation (enhancing) of NMDAR associated with long-term potentiation
8) Confidence 0.53 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.22 Pain Relevance 0.09
In addition, we used mice with a disrupted NMDAR1 gene that lack functional NMDARs (NR1-/-) to assess the physiological role of NMDARs.
Positive_regulation (disrupted) of NMDAR1 gene
9) Confidence 0.50 Published 1996 Journal J. Neurosci. Section Abstract Doc Link 8764653 Disease Relevance 0 Pain Relevance 0.15
Our results demonstrate conclusively that the postsynaptic NR1 receptor subunit in the lumbar dorsal horn of the spinal cord is required for central sensitization, the central facilitation of pain transmission produced by peripheral injury.
Positive_regulation (required) of NR1 in spinal cord associated with pain, central sensitization, injury, dorsal horn and spinal cord
10) Confidence 0.50 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12832526 Disease Relevance 0.85 Pain Relevance 0.73
Glutamate released from presynaptic sites by TBS activates N-methyl-D-aspartate receptor (NMDAR) at postsynaptic sites, followed by a Ca2+ influx.
Positive_regulation (activates) of NMDAR associated with glutamate and nmda receptor
11) Confidence 0.49 Published 2007 Journal Gene Regulation and Systems Biology Section Body Doc Link PMC2759147 Disease Relevance 0 Pain Relevance 0.24
Using these antagonists, recent studies have shown that NR2A-containg NMDARs are required for LTP, whereas NR2B NMDARs are required for LTD [11,12].
Positive_regulation (required) of NMDAR associated with antagonist
12) Confidence 0.49 Published 2007 Journal Mol Pain Section Body Doc Link PMC1871573 Disease Relevance 0.28 Pain Relevance 0.45
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 (activation) of NMDAR
13) Confidence 0.45 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.14
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 (activation) of NMDAR
14) Confidence 0.45 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.07
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).
Positive_regulation (induced) of NMDAR
15) Confidence 0.45 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0.06 Pain Relevance 0.10
In the present study, we show that SK channels mediating a component of the IAHP are directly modulated by M1 receptors (Figure 6) and that blockade of SK channels with apamin occludes the action of M1 receptor activation on NMDAR function (Figure 6) and LTP induction (Figure 8).
Positive_regulation (induction) of NMDAR associated with long-term potentiation
16) Confidence 0.45 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.38
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).
Positive_regulation (activation) of NMDAR in spines
17) Confidence 0.45 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 (activation) of NMDAR associated with long-term potentiation
18) Confidence 0.45 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.26
NR1 expression is not altered in the dark-reared visual cortex [24,25] but contrarily, an intraocular injection of tetrodotoxin (TTX) does increase NR1-antibody binding in layer IV of the cortical column driven by the blocked eye [41].
Positive_regulation (increase) of NR1 in eye associated with tetrodotoxin
19) Confidence 0.43 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC32198 Disease Relevance 0 Pain Relevance 0.13
When injected into the PAG 10 min prior local NMDA injection (0.02 nmol/0.1 microl), NPLA (0.4 nmol/0.1 microl) was able to revert the anxiogenic-like effect of glutamate-NMDA receptor activation.
Positive_regulation (activation) of glutamate-NMDA receptor associated with glutamate, nmda receptor and central grey
20) Confidence 0.42 Published 2008 Journal Brain Res. Section Abstract Doc Link 18793618 Disease Relevance 0.98 Pain Relevance 0.80

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