INT197207

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Context Info
Confidence 0.43
First Reported 2006
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 6
Disease Relevance 1.91
Pain Relevance 3.50

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

transport (Grik1) plasma membrane (Grik1)
Anatomy Link Frequency
synapses 2
spinal 1
neurons 1
Grik1 (Mus musculus)
Pain Link Frequency Relevance Heat
Anterior cingulate cortex 126 99.10 Very High Very High Very High
Analgesic 5 98.60 Very High Very High Very High
gABA 71 98.48 Very High Very High Very High
Glutamate 18 98.44 Very High Very High Very High
amygdala 133 97.60 Very High Very High Very High
substantia gelatinosa 171 97.40 Very High Very High Very High
intrathecal 3 94.72 High High
Action potential 94 92.80 High High
Pyramidal cell 87 91.80 High High
antagonist 36 91.28 High High
Disease Link Frequency Relevance Heat
Nociception 25 98.80 Very High Very High Very High
Targeted Disruption 28 96.70 Very High Very High Very High
INFLAMMATION 13 87.44 High High
Inflammatory Pain 3 74.64 Quite High
Nervous System Injury 34 70.56 Quite High
Pain 30 70.52 Quite High
Anxiety Disorder 55 51.40 Quite High
Epilepsy 3 51.16 Quite High
Neuropathic Pain 58 44.56 Quite Low
Injury 14 18.32 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results indicated that genetic deletion of GluR5 KARs might have no effect on the basal synaptic transmission in SG neurons.


Negative_regulation (deletion) of GluR5 in neurons associated with substantia gelatinosa
1) Confidence 0.43 Published 2006 Journal Mol Pain Section Body Doc Link PMC1570342 Disease Relevance 0.05 Pain Relevance 0.44
Therefore, the blockade of GluR5 at the spinal level would have an analgesic effect.
Negative_regulation (blockade) of GluR5 in spinal associated with analgesic
2) Confidence 0.43 Published 2006 Journal Mol Pain Section Body Doc Link PMC1570342 Disease Relevance 0.86 Pain Relevance 0.80
However, the effect of ATPA on the frequency of either sIPSCs or mIPSCs was abolished in GluR5-/- mice.
Negative_regulation (abolished) of GluR5
3) Confidence 0.37 Published 2006 Journal Mol Pain Section Abstract Doc Link PMC1570342 Disease Relevance 0.05 Pain Relevance 0.50
Genetic deletion of GluR5 or pharmacological blockade of GluR5 could significantly reduce the tonic GABA current.
Negative_regulation (blockade) of GluR5 associated with gaba
4) Confidence 0.34 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1766473 Disease Relevance 0 Pain Relevance 0.59
Taking advantage of transgenic and gene knockout mice, recent studies reveal novel molecular and synaptic mechanisms for synaptic transmission and plasticity in the ACC [13,15,27,33,34] For example, using genetic deletion of GluR5, Glur6, or GluR5&6, Wu et al (2005a) demonstrated that glutamate kainate receptor GluR5 and 6 contribute to excitatory synaptic transmission in the synapses of layer II/III ACC.
Negative_regulation (deletion) of GluR5 in synapses associated with targeted disruption, glutamate and anterior cingulate cortex
5) Confidence 0.21 Published 2009 Journal Mol Pain Section Body Doc Link PMC2807858 Disease Relevance 0.47 Pain Relevance 0.58
Taking advantage of transgenic and gene knockout mice, recent studies reveal novel molecular and synaptic mechanisms for synaptic transmission and plasticity in the ACC [13,15,27,33,34] For example, using genetic deletion of GluR5, Glur6, or GluR5&6, Wu et al (2005a) demonstrated that glutamate kainate receptor GluR5 and 6 contribute to excitatory synaptic transmission in the synapses of layer II/III ACC.
Negative_regulation (deletion) of GluR5 in synapses associated with targeted disruption, glutamate and anterior cingulate cortex
6) Confidence 0.19 Published 2009 Journal Mol Pain Section Body Doc Link PMC2807858 Disease Relevance 0.47 Pain Relevance 0.58

General Comments

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