INT64918

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Context Info
Confidence 0.74
First Reported 1995
Last Reported 2010
Negated 3
Speculated 1
Reported most in Body
Documents 108
Total Number 111
Disease Relevance 29.95
Pain Relevance 29.67

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

transport (Gria2) endoplasmic reticulum (Gria2) plasma membrane (Gria2)
protein complex (Gria2)
Anatomy Link Frequency
neurons 12
hippocampus 9
synapses 6
spinal 4
dorsal horn 4
Gria2 (Mus musculus)
Pain Link Frequency Relevance Heat
Anterior cingulate cortex 456 100.00 Very High Very High Very High
Glutamate receptor 430 100.00 Very High Very High Very High
Glutamate 315 100.00 Very High Very High Very High
Thalamus 70 100.00 Very High Very High Very High
long-term potentiation 1622 99.98 Very High Very High Very High
addiction 42 99.92 Very High Very High Very High
Hippocampus 1111 99.84 Very High Very High Very High
Dorsal horn 368 99.84 Very High Very High Very High
spinal dorsal horn 152 99.84 Very High Very High Very High
nMDA receptor 691 99.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Thiamine Deficiency 434 99.80 Very High Very High Very High
Bone Cancer 123 99.74 Very High Very High Very High
Depression 520 99.60 Very High Very High Very High
INFLAMMATION 277 99.48 Very High Very High Very High
Nociception 524 99.36 Very High Very High Very High
Injury 130 98.96 Very High Very High Very High
Anxiety Disorder 787 98.60 Very High Very High Very High
Inflammatory Pain 199 98.50 Very High Very High Very High
Targeted Disruption 973 98.36 Very High Very High Very High
Absence Epilepsy 75 98.20 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These combined results demonstrate that while GluR2 expression is significantly reduced from the expected regions of the dorsal hippocampus of mutant mice this loss does not lead to cell death in mice at eight weeks of age.
Gene_expression (expression) of GluR2 in dorsal associated with hippocampus and death
1) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.26 Pain Relevance 0.24
We also noted no difference in expression of GluR2 in the amygdala between GluR2-cKO mice and controls.
Gene_expression (expression) of GluR2 in amygdala associated with amygdala
2) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.05 Pain Relevance 0.28
As expected, we observed a significant loss of GluR2 expression in dorsal CA1 pyramidal neurons in the GluR2-cKO mice at 6 weeks and 8 weeks of age compared to control mice of the same age (57.7±3.0% vs 91.8±1.4% at 6 weeks and 52.8±2.2% vs 95.2±0.4% at 8 weeks; p values<.05).
Gene_expression (expression) of GluR2 in dorsal associated with pyramidal cell
3) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0 Pain Relevance 0.26
Consequently, a potential mechanism for NMDAR-independent learning and plasticity in the hippocampus is the expression and activation of GluR2-lacking (Ca2+-permeable) AMPARs.
Gene_expression (expression) of GluR2 in hippocampus associated with hippocampus
4) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.06 Pain Relevance 0.34
In fact, a number of different experiences (e.g. learning, drug exposure, sensory deprivation) increase the expression of GluR2-lacking Ca2+-permeable AMPARs [9], [51], [52], [53], [54].
Gene_expression (expression) of GluR2
5) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.26 Pain Relevance 0.12
As one of three classes of ionotropic glutamate receptors, AMPA receptors were cloned and expressed in recombinant systems in the late 1980s.
Gene_expression (expressed) of AMPA associated with glutamate receptor
6) Confidence 0.69 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.24 Pain Relevance 0.32
In an animal model of complete Freund's adjuvant (CFA)-induced persistent inflammatory pain, Park et al. found that CFA-induced inflammation did not change the total expression or distribution of AMPA receptor subunits, GluR1 and GluR2 in spinal dorsal horn, but did alter their subcellular distribution.
Gene_expression (expression) of GluR2 in dorsal horn associated with inflammation, spinal dorsal horn and ipn
7) Confidence 0.69 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.45 Pain Relevance 0.58
In an animal model of complete Freund's adjuvant (CFA)-induced persistent inflammatory pain, Park et al. found that CFA-induced inflammation did not change the total expression or distribution of AMPA receptor subunits, GluR1 and GluR2 in spinal dorsal horn, but did alter their subcellular distribution.
Gene_expression (expression) of AMPA receptor in dorsal horn associated with inflammation, spinal dorsal horn and ipn
8) Confidence 0.69 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.45 Pain Relevance 0.57
The expression of GluR2 was observed throughout the dorsal horn and was abundant in inner lamina II and sparse in outer lamina II.
Gene_expression (expression) of GluR2 in lamina associated with dorsal horn
9) Confidence 0.69 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0 Pain Relevance 0.46
In the CNS, GluR1 and GluR2 subunits are ubiquitously expressed and are present in most AMPA receptors in the adult mammalian CNS.
Gene_expression (expressed) of GluR2 associated with central nervous system
10) Confidence 0.69 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0 Pain Relevance 0.34
Thus, our experiments using GluA1/2 KO mice suggest that the AMPA receptor subunits, GluA1 and GluA2, act differentially in ACC LTP.


Gene_expression (act) of AMPA associated with long-term potentiation and anterior cingulate cortex
11) Confidence 0.65 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0.08 Pain Relevance 0.60
Thus, our experiments using GluA1/2 KO mice suggest that the AMPA receptor subunits, GluA1 and GluA2, act differentially in ACC LTP.


Gene_expression (act) of GluA2 associated with long-term potentiation and anterior cingulate cortex
12) Confidence 0.65 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0.08 Pain Relevance 0.60
The other two subunits of AMPA receptor, GluA3 and GluA4 express at relative lower levels [21,22].
Gene_expression (express) of AMPA
13) Confidence 0.65 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0.31 Pain Relevance 0.81
GluA1 and GluA2 subunits in cortical LTP
Gene_expression (subunits) of GluA2 associated with long-term potentiation
14) Confidence 0.65 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0 Pain Relevance 0.50
In order to assess if there was any change in the percentage of cells expressing GluR2 during this time period in mice within the same genotype, we compared percentage of cells that contained GluR2 mRNA at these two time points within each genotype, at all five anatomic regions analyzed.
Gene_expression (expressing) of GluR2 in anatomic regions
15) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0 Pain Relevance 0.16
Consistent with the notion that the larger LTP observed in GluR2-cKOs is associated with Ca2+ influx via GluR2-lacking AMPARs, HFS induced a significant LTP in slices from GluR2-cKO mice bathed in ACSF containing the NMDAR antagonist D-APV (100 µM; 60 minutes post-HFS fEPSPs were potentiated to 134±4% of baseline in cKO slices, n?
Gene_expression (observed) of GluR2 associated with antagonist and long-term potentiation
16) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.12 Pain Relevance 0.38
Our results demonstrate that deletion of GluR2 in the CA1 region of the hippocampus produces AMPAR-mediated plasticity that impairs learning and memory.
Gene_expression (deletion) of GluR2 in hippocampus associated with hippocampus
17) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.31 Pain Relevance 0.13
AMPA receptors lacking the GluR2 subunit are resistant to blockade by barbiturates in vitro.
Neg (lacking) Gene_expression (lacking) of AMPA
18) Confidence 0.64 Published 2001 Journal Anesthesiology Section Abstract Doc Link 11374610 Disease Relevance 0 Pain Relevance 0.17
GluR2 subunit is expressed abundantly in the hippocampal pyramidal neurons and Purkinje cells in the cerebellum [17].
Gene_expression (expressed) of GluR2 in Purkinje cells associated with pyramidal cell
19) Confidence 0.61 Published 2004 Journal BMC Med Genet Section Body Doc Link PMC411038 Disease Relevance 0.05 Pain Relevance 0.43
Since GluR2 is widely expressed in the CNS, a majority of AMPA receptors in the CNS present low permeability for Ca2+ influx.
Gene_expression (expressed) of GluR2 associated with central nervous system
20) Confidence 0.60 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.08 Pain Relevance 0.50

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