INT111948

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Context Info
Confidence 0.61
First Reported 2001
Last Reported 2010
Negated 2
Speculated 3
Reported most in Abstract
Documents 23
Total Number 26
Disease Relevance 7.55
Pain Relevance 12.03

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

cytosol (Gria1) transport (Gria1) endoplasmic reticulum (Gria1)
plasma membrane (Gria1) protein complex (Gria1)
Anatomy Link Frequency
spinal 4
visceral 1
molecular layer 1
tectum 1
spinal cord 1
Gria1 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate receptor 129 100.00 Very High Very High Very High
agonist 20 99.96 Very High Very High Very High
Neurotransmitter 20 99.86 Very High Very High Very High
long-term potentiation 98 99.64 Very High Very High Very High
Cancer pain 17 99.64 Very High Very High Very High
Glutamate 98 99.52 Very High Very High Very High
Somatosensory cortex 13 99.46 Very High Very High Very High
Dorsal horn 39 99.20 Very High Very High Very High
Spinal sensitization 26 99.20 Very High Very High Very High
Pain 68 99.12 Very High Very High Very High
Disease Link Frequency Relevance Heat
Bone Cancer 41 99.84 Very High Very High Very High
Alzheimer's Dementia 43 98.48 Very High Very High Very High
Pain 74 98.16 Very High Very High Very High
Death 100 97.92 Very High Very High Very High
Syndrome 55 97.20 Very High Very High Very High
Drug Dependence 5 96.24 Very High Very High Very High
Neuropathic Pain 47 95.28 Very High Very High Very High
Targeted Disruption 159 93.96 High High
Sprains And Strains 28 93.24 High High
Neurological Disease 3 86.80 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, it remains to be tested if the increased amounts of GluR1 observed in this study are due to new protein synthesis or to a translocation from some intracellular compartment to the synaptic membrane [27,29].
Positive_regulation (increased) of GluR1
1) Confidence 0.61 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC32198 Disease Relevance 0 Pain Relevance 0.07
The demonstration that GluR1 expression is increased in the retina of the rdta mouse where a rod photoreceptor-mediated visual input is missing is consistent with a previous report in which the level of GluR1 is increased in the deafferented tectum [64,65].
Positive_regulation (increased) of GluR1 in tectum
2) Confidence 0.61 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC32198 Disease Relevance 0 Pain Relevance 0.04
In the somatosensory cortex, Frey et al reported that GluA1 is not required for the LTP in the layer II/III barrel cortex [24].
Neg (not) Positive_regulation (required) of GluA1 in barrel cortex associated with somatosensory cortex and long-term potentiation
3) Confidence 0.50 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0.06 Pain Relevance 0.60
Conversely, the level of GluR1 was significantly reduced in the crude cytosolic fraction and increased in the crude membrane fraction from the ipsilateral L4-5 dorsal horn at 24 hour post-CFA injection [5].
Positive_regulation (increased) of GluR1 in dorsal horn associated with dorsal horn
4) Confidence 0.42 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.45 Pain Relevance 0.51
In spinal neurons, intra-thecal application of a CaMKII inhibitor, KN-93, before the painful visceral stimulus, apparently inhibits the GluR1 accumulation in the plasma membrane fraction [24].
Positive_regulation (accumulation) of GluR1 in visceral associated with pain
5) Confidence 0.42 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.48 Pain Relevance 0.62
The GluR1 receptor subunit and its phosphorylation are simultaneously increased in retinae of the rdta mice.


Positive_regulation (increased) of GluR1
6) Confidence 0.41 Published 2001 Journal BMC Neurosci Section Abstract Doc Link PMC32198 Disease Relevance 0.07 Pain Relevance 0.21
Zhou et al. [51] observed a rapid up-regulation of GluR1 mRNA in the lumbar dorsal horn following injection of complete Freund's adjuvant into the hindpaw, while Fang et al. [52] reported phosphorylation of this subunit at both S831 and S845 sites in Western blots of spinal cord tissue after intradermal capsaicin injection.
Positive_regulation (regulation) of GluR1 in spinal cord associated with qutenza, dorsal horn and spinal cord
7) Confidence 0.40 Published 2008 Journal Mol Pain Section Body Doc Link PMC2248168 Disease Relevance 0.10 Pain Relevance 0.55
The metabotropic glutamate receptor type 1 (mGluR1)-mediated slow synaptic response was induced by repetitive stimulation of PFs (50 Hz, 1–20 times) in the molecular layer in the presence of 10 µM ?
Positive_regulation (induced) of glutamate receptor in molecular layer associated with glutamate receptor
8) Confidence 0.28 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386150 Disease Relevance 0 Pain Relevance 0.22
Phosphorylation of GluR1 at Ser 831 and Ser 845 sites is important for GluR1 trafficking [50].
Positive_regulation (important) of GluR1
9) Confidence 0.28 Published 2010 Journal Mol Brain Section Body Doc Link PMC2822766 Disease Relevance 0.20 Pain Relevance 0.24
We investigated whether this spinal sensitization involves activation and phosphorylation of calcium-dependent protein kinases (PKA, PKC and CaMKIIalpha), and examined if the noxious stimulus increases phosphorylated AMPA GLUR1 (pGLUR1 Ser-845 and pGLUR1 Ser-831).
Spec (examined) Positive_regulation (increases) of GLUR1 in spinal associated with spinal sensitization
10) Confidence 0.21 Published 2005 Journal Pain Section Abstract Doc Link 16150547 Disease Relevance 0.50 Pain Relevance 0.72
In order to determine whether a similar effect of GluR activation occurs for oligodendrocytes, dispersed cultures were treated with sub lethal doses of KA and the amount of COX-2 expression examined by immunofluorescent confocal microscopy.
Spec (whether) Positive_regulation (activation) of GluR in oligodendrocytes associated with glutamate receptor
11) Confidence 0.19 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2873241 Disease Relevance 0.35 Pain Relevance 0.24
Pretreatment with a selective calcium-permeable AMPA/KA receptor antagonist (5nmol joro spider toxin), but not an NMDA receptor antagonist (25nmol d-2-amino-5-phosphonovalerate, AP-5), blocked thermal stimulus-evoked increases in phosphorylated PKA and PKC, in addition to increased cytosolic GLUR1.
Positive_regulation (increased) of GLUR1 associated with nmda receptor antagonist and antagonist
12) Confidence 0.19 Published 2005 Journal Pain Section Abstract Doc Link 16150547 Disease Relevance 0.28 Pain Relevance 0.53
It is unknown why the GluR?
Positive_regulation (why) of GluR
13) Confidence 0.17 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2615205 Disease Relevance 0.08 Pain Relevance 0.10
These findings indicate that spinal sensitization in the thermal stimulus model does not involve CaMKIIalpha activation or AMPA GLUR1 receptor phosphorylation, and differs from that occurring in NMDAr-dependent pain states.
Positive_regulation (activation) of GLUR1 in spinal associated with pain and spinal sensitization
14) Confidence 0.15 Published 2005 Journal Pain Section Abstract Doc Link 16150547 Disease Relevance 0.36 Pain Relevance 0.49
We investigated whether this spinal sensitization involves activation and phosphorylation of calcium-dependent protein kinases (PKA, PKC and CaMKIIalpha), and examined if the noxious stimulus increases phosphorylated AMPA GLUR1 (pGLUR1 Ser-845 and pGLUR1 Ser-831).
Spec (examined) Positive_regulation (increases) of GLUR1 in spinal associated with spinal sensitization
15) Confidence 0.15 Published 2005 Journal Pain Section Abstract Doc Link 16150547 Disease Relevance 0.50 Pain Relevance 0.72
Although thermal stimulation did not change either pGLUR1 Ser-845 or pGLUR1 Ser-831, it was associated with an increase in cytosolic total GLUR1.
Positive_regulation (increase) of GLUR1
16) Confidence 0.15 Published 2005 Journal Pain Section Abstract Doc Link 16150547 Disease Relevance 0.37 Pain Relevance 0.70
These findings indicate that spinal sensitization in the thermal stimulus model does not involve CaMKIIalpha activation or AMPA GLUR1 receptor phosphorylation, and differs from that occurring in NMDAr-dependent pain states.
Neg (not) Positive_regulation (involve) of GLUR1 in spinal associated with pain and spinal sensitization
17) Confidence 0.15 Published 2005 Journal Pain Section Abstract Doc Link 16150547 Disease Relevance 0.36 Pain Relevance 0.50
Activation of the NMDA subtype of the glutamate receptor has been implicated as an anti-opioid system in the development of morphine analgesic tolerance and dependence.
Positive_regulation (Activation) of glutamate receptor associated with addiction, analgesic, glutamate receptor, tolerance, opioid and morphine
18) Confidence 0.15 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12878694 Disease Relevance 0.17 Pain Relevance 1.10
Glutamate is an important extracellular neurotransmitter which activates glutamate receptor and induces a series of signal transduction to regulate the development of opioid tolerance.
Positive_regulation (activates) of glutamate receptor associated with neurotransmitter, glutamate, glutamate receptor, tolerance and opioid
19) Confidence 0.14 Published 2004 Journal Acta anaesthesiologica Taiwanica : official journal of the Taiwan Society of Anesthesiologists Section Abstract Doc Link 15346705 Disease Relevance 0.22 Pain Relevance 1.63
Ca(2+) levels within ES cell-derived neurons increased in response to glutamate receptor agonists l-glutamate, AMPA, N-methyl-d-aspartate (NMDA) and kainic acid and to acetylcholine, ATP and dopamine.
Positive_regulation (response) of glutamate receptor in neurons associated with dopamine, glutamate, glutamate receptor and agonist
20) Confidence 0.13 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15610154 Disease Relevance 0 Pain Relevance 0.74

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