INT96298

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Context Info
Confidence 0.57
First Reported 2001
Last Reported 2010
Negated 1
Speculated 2
Reported most in Body
Documents 25
Total Number 27
Disease Relevance 10.61
Pain Relevance 9.70

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
hippocampus 2
juvenile 1
neurons 1
striatum 1
dorsal horn 1
Gria1 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate receptor 136 100.00 Very High Very High Very High
long-term potentiation 341 99.90 Very High Very High Very High
Hippocampus 122 99.84 Very High Very High Very High
amygdala 187 99.48 Very High Very High Very High
nMDA receptor antagonist 7 99.06 Very High Very High Very High
Inflammation 48 98.90 Very High Very High Very High
depression 108 98.74 Very High Very High Very High
Anterior cingulate cortex 164 98.00 Very High Very High Very High
antagonist 14 97.80 Very High Very High Very High
Dorsal horn 32 97.72 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 155 100.00 Very High Very High Very High
Anxiety Disorder 561 99.62 Very High Very High Very High
INFLAMMATION 46 98.90 Very High Very High Very High
Depression 108 98.74 Very High Very High Very High
Cognitive Disorder 61 97.60 Very High Very High Very High
Neuropathic Pain 18 96.32 Very High Very High Very High
Shock 79 95.24 Very High Very High Very High
Body Weight 14 93.00 High High
Drug Dependence 10 90.60 High High
Pain 76 88.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Complete loss of GluR1 led to a severe deficit in tone and context forms of delay and trace fear conditioning.
Negative_regulation (loss) of GluR1 associated with anxiety disorder
1) Confidence 0.57 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.48 Pain Relevance 0.04
GluR1 KO mice are impaired on hippocampus-dependent tasks such as T-maze spatial learning (Bannerman et al., 2006).
Negative_regulation (impaired) of GluR1 in hippocampus associated with hippocampus
2) Confidence 0.57 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.64 Pain Relevance 0.33
GluR1 KO were impaired on a (multi-trial) trace fear conditioning paradigm that is sensitive to hippocampal inactivation in mice (Misane et al., 2005).
Negative_regulation (impaired) of GluR1 associated with anxiety disorder
3) Confidence 0.50 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.67 Pain Relevance 0.33
We found a substantial decrease in the levels of GluR1 associated with clathrin.
Negative_regulation (decrease) of GluR1
4) Confidence 0.44 Published 2007 Journal Mol. Cell Proteomics Section Abstract Doc Link 17028301 Disease Relevance 0 Pain Relevance 0.56
Present data predict that loss of GluR1 function in amygdala neurons would cause deficits in other cognitive tasks mediated by this brain region.
Negative_regulation (loss) of GluR1 in neurons associated with cognitive disorder and amygdala
5) Confidence 0.42 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.35 Pain Relevance 0.25
A major question for future studies therefore will be whether GluR1 HET are similarly impaired on other tasks requiring rapid and memory formation.


Spec (whether) Negative_regulation (impaired) of GluR1
6) Confidence 0.42 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.60 Pain Relevance 0.04
Thus, while complete loss of GluR1 severely disrupts the formation of associative fear memories, partial loss of GluR1 appears to produce a more subtle fear-learning deficit that manifest after a single learning event but which can be overcome when multiple learning opportunities are available.
Negative_regulation (loss) of GluR1 associated with anxiety disorder
7) Confidence 0.42 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.68 Pain Relevance 0.12
Thus, while complete loss of GluR1 severely disrupts the formation of associative fear memories, partial loss of GluR1 appears to produce a more subtle fear-learning deficit that manifest after a single learning event but which can be overcome when multiple learning opportunities are available.
Negative_regulation (loss) of GluR1 associated with anxiety disorder
8) Confidence 0.42 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.67 Pain Relevance 0.11
In the present study, we sought to extend these findings by comparing mice completely lacking GluR1 (KO) and mice with GluR1 haploinsufficiency (heterozygous, HET) on various forms of fear conditioning.
Negative_regulation (lacking) of GluR1 associated with anxiety disorder
9) Confidence 0.41 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.68 Pain Relevance 0.19
The first line is entirely deficient in glutamate receptor-A (GluR-A) subunits (A-/- knock-out line) and, in the second one, the Q582 residue of GluR-A subunits is replaced by an arginine residue (R/R mutants), which reduces the calcium permeability and channel conductance of the receptors containing this mutated subunit.
Negative_regulation (replaced) of GluR-A associated with targeted disruption and glutamate receptor
10) Confidence 0.41 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11404432 Disease Relevance 0.25 Pain Relevance 0.69
AMPA receptor-mediated EPSCs are reduced in GluA1-/- mice
Negative_regulation (reduced) of GluA1
11) Confidence 0.37 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0 Pain Relevance 0.37
This result is consistent with the previous reports that LTP was impaired in GluA1-/- mice in the hippocampus [27,54].
Negative_regulation (impaired) of GluA1 in hippocampus associated with hippocampus and long-term potentiation
12) Confidence 0.37 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0 Pain Relevance 0.55
However, the contribution of a hippocampal deficit to the trace conditioning impairment in these mice cannot be excluded and would in fact be congruent with previously observed GluR1 KO impairments in hippocampal synaptic plasticity and hippocampal-mediated forms of learning such as spatial working and reference memory (Mack et al., 2001; Schmitt et al., 2005; Zamanillo et al., 1999).
Negative_regulation (impairments) of GluR1
13) Confidence 0.37 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.48 Pain Relevance 0.23
Although the molecular underpinnings of such a one-trial versus multi-trial dissociation are not clear, the relative lack of a GluR1 in HET mice could be insufficient to permit the necessary rapid synaptic incorporation of GluR1 during a one-trial learning event.
Negative_regulation (lack) of GluR1
14) Confidence 0.37 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525858 Disease Relevance 0.78 Pain Relevance 0.03
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].
Negative_regulation (reduced) of GluR1 in dorsal horn associated with dorsal horn
15) Confidence 0.35 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.45 Pain Relevance 0.51
The second tonic inflammatory phase response in the formalin test was significantly reduced in glutamate receptor epsilon1 knockout epsilon1(-/-) mice, but not in glutamate receptor epsilon4(-/-) when compared with wild-type mice.
Neg (not) Negative_regulation (reduced) of glutamate receptor associated with targeted disruption, inflammation and glutamate receptor
16) Confidence 0.33 Published 2005 Journal Neuroreport Section Abstract Doc Link 16189474 Disease Relevance 0.87 Pain Relevance 1.21
Approximately 10% of puncta were found to lack both GluR1- and GluR3-immunoreactivity, and these may correspond to those that express the GluR4 subunit.
Negative_regulation (lack) of GluR1
17) Confidence 0.32 Published 2008 Journal Mol Pain Section Body Doc Link PMC2248168 Disease Relevance 0.06 Pain Relevance 0.25
Therefore, major effects on LTP as a consequence of the observed reduction of AMPA subunit GluR1 by approximately 30% are not expected.
Negative_regulation (reduction) of GluR1 associated with long-term potentiation
18) Confidence 0.29 Published 2007 Journal Environ Health Perspect Section Body Doc Link PMC1892123 Disease Relevance 0.18 Pain Relevance 0.52
We found that LTP is still impaired in neurabin KO mice, suggesting that decreased in “primed” pool of GluR1 is not the mechanism.
Negative_regulation (decreased) of GluR1 associated with targeted disruption and long-term potentiation
19) Confidence 0.26 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2169299 Disease Relevance 1.25 Pain Relevance 0.70
We also identified a reduced number of GluR1-immunoreactive puncta in the striatum radiatum.
Negative_regulation (reduced) of GluR1 in striatum
20) Confidence 0.26 Published 2010 Journal Mol Autism Section Body Doc Link PMC3019144 Disease Relevance 0 Pain Relevance 0

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