INT231293

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Context Info
Confidence 0.45
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 10
Disease Relevance 3.95
Pain Relevance 3.38

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

transport (Grin2d) plasma membrane (Grin2d)
Anatomy Link Frequency
frontal cortex 2
synapse 1
Grin2d (Mus musculus)
Pain Link Frequency Relevance Heat
allodynia 8 99.96 Very High Very High Very High
nMDA receptor 973 98.96 Very High Very High Very High
Glutamate 189 95.08 Very High Very High Very High
Pain 3 93.04 High High
Hyperalgesia 5 92.00 High High
agonist 101 91.88 High High
Hippocampus 493 91.48 High High
long-term potentiation 184 90.16 High High
Inflammation 14 89.32 High High
antagonist 160 88.52 High High
Disease Link Frequency Relevance Heat
Aging 798 100.00 Very High Very High Very High
Neuropathic Pain 8 99.96 Very High Very High Very High
Targeted Disruption 37 99.32 Very High Very High Very High
Urological Neuroanatomy 100 99.16 Very High Very High Very High
Disease 62 98.60 Very High Very High Very High
Cognitive Disorder 175 98.52 Very High Very High Very High
Pain 8 93.04 High High
Hyperalgesia 5 92.00 High High
INFLAMMATION 14 89.32 High High
Stress 16 85.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Consistent with such a mechanism, siRNA depletion of NR2D subunits greatly diminished (and accelerated) the NMDA currents seen in PrP-null mouse cultures.
Negative_regulation (depletion) of NR2D
1) Confidence 0.45 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2364707 Disease Relevance 0 Pain Relevance 0.04
Consistent with such a mechanism, siRNA depletion of NR2D subunits greatly diminished (and accelerated) the NMDA currents seen in PrP-null mouse cultures.
Negative_regulation (diminished) of NR2D
2) Confidence 0.33 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2364707 Disease Relevance 0 Pain Relevance 0.04
In this context, it is possible that these receptors may contribute to development of NR2D-dependent allodynia.


Negative_regulation (development) of NR2D-dependent associated with allodynia
3) Confidence 0.28 Published 2008 Journal Mol Pain Section Body Doc Link PMC2572590 Disease Relevance 0.47 Pain Relevance 0.66
These studies suggest that age-related reductions in the levels of the GluN2B subunit are likely to contribute to memory impairment in aged individuals.
Negative_regulation (reductions) of GluN2B associated with cognitive disorder
4) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.65 Pain Relevance 0.30
A study by Calon et al. (2005) showed that in a mouse model of AD with n-3 PUFA deficiency, the expression levels of GluN1, GluN2A and GluN2B subunits are significantly decreased compared to non-transgenic mice.
Negative_regulation (decreased) of GluN2B associated with targeted disruption and disease
5) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.63 Pain Relevance 0.07
An age-related decline in the GluN2B subunit within the synapse, with little or no change in the GluN2A (Magnusson, 2000; Magnusson et al., 2002) and GluN1 subunits could lead to a synaptic population of NMDA receptors that have decreased agonist affinity, faster kinetics, and reduced LTP associated with binding of calcium calmodulin kinase II (Kutsuwada et al., 1992; Monyer et al., 1992; Yamazaki et al., 1992; Ishii et al., 1993; Barria and Malinow, 2005) than in the young adult.
Negative_regulation (decline) of GluN2B in synapse associated with nmda receptor, agonist and long-term potentiation
6) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.05 Pain Relevance 0.33
Insulin-like growth factor 1 (IGF-1) alleviates the decline in both GluN2A and GluN2B subunits seen in older F344XBN rats (Sonntag et al., 2000).
Negative_regulation (decline) of GluN2B
7) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.54 Pain Relevance 0.54
The percent decline during aging in the GluN2B subunit mRNA across different cortical and hippocampal subregions shows an association with changes in the binding of [3H]glutamate to NMDA receptors, while the decreases with age in the GluN1 subunit mRNA are more related to age-related declines in [3H]CPP binding in the same regions (Magnusson, 2000).
Negative_regulation (decline) of GluN2B associated with glutamate, aging and nmda receptor
8) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.62 Pain Relevance 0.73
The declines in the mRNA expression of the GluN2B subunit in the frontal cortex show a pattern that suggests that the aging change may be a continuation of the programmed developmental decline of the GluN2B subunit (Ontl et al., 2004).
Negative_regulation (decline) of GluN2B in frontal cortex associated with aging and urological neuroanatomy
9) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.63 Pain Relevance 0.33
There was also a decrease in the low affinity and an increase in the high affinity ifenprodil components in oocytes injected with aged mRNA (Kuehl-Kovarik et al., 2000), which is consistent with the findings of decreased GluN2B subunit mRNA in the frontal cortex of aged mice (Magnusson, 2000, 2001).
Negative_regulation (decreased) of GluN2B in frontal cortex associated with urological neuroanatomy
10) Confidence 0.02 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874396 Disease Relevance 0.36 Pain Relevance 0.33

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