INT244375

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Context Info
Confidence 0.04
First Reported 2008
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 11
Disease Relevance 5.29
Pain Relevance 3.32

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

Anatomy Link Frequency
neurons 10
Cl (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 506 99.98 Very High Very High Very High
Inflammation 198 99.84 Very High Very High Very High
Hyperalgesia 132 99.32 Very High Very High Very High
Neuropathic pain 11 99.32 Very High Very High Very High
GABAergic 55 98.60 Very High Very High Very High
nociceptor 132 97.28 Very High Very High Very High
gABA 165 93.52 High High
substance P 110 86.12 High High
Inflammatory response 22 83.04 Quite High
Inflammatory stimuli 22 78.48 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 726 99.84 Very High Very High Very High
Neurological Disease 11 99.58 Very High Very High Very High
Hyperalgesia 132 99.32 Very High Very High Very High
Neuropathic Pain 55 99.32 Very High Very High Very High
Nociception 132 98.12 Very High Very High Very High
Epilepsy 11 95.32 Very High Very High Very High
Peripheral Arterial Disease 44 87.68 High High
Ganglion Cysts 22 50.00 Quite Low
Targeted Disruption 11 42.12 Quite Low
Pain 22 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In which way could a general increase of [Cl-]i in DRG neurons contribute to inflammatory hyperalgesia?
Positive_regulation (contribute) of Positive_regulation (increase) of Cl in neurons associated with hyperalgesia and inflammation
1) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.47 Pain Relevance 0.60
To test whether NKCC1 phosphorylation may contribute to the early rise of Cl- levels (< 3 hr), we stained 9 DRG sections from 3 animals with an antibody raised specifically against the phosphorylated form of NKCC1 (p-NKCC1).
Spec (may) Positive_regulation (contribute) of Positive_regulation (rise) of Cl
2) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.22 Pain Relevance 0.11
These data demonstrate that the inflammatory mediators induce the phosphorylation of NKCC1 in DRG neurons and suggest that this phosphorylation causes the early (< 3 hr) phase of enhanced Cl- accumulation observed by 2P-FLIM in response to the stimulus.


Positive_regulation (causes) of Positive_regulation (accumulation) of Cl in neurons associated with inflammatory mediators
3) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.41 Pain Relevance 0.24
Moreover, nociceptive lamina-I dorsal-horn neurons in a model of neuropathic pain display a depolarized ECl due to increased Cl- accumulation [31] and the consequent occurrence of excitatory Cl- currents.
Positive_regulation (increased) of Positive_regulation (accumulation) of Cl in neurons associated with nociception and neuropathic pain
4) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.75 Pain Relevance 0.37
This observation suggests that the enhanced Cl- accumulation is not the consequence of transcriptional upregulation of NKCC1 or the downregulation of KCC2 transcription.
Positive_regulation (enhanced) of Positive_regulation (accumulation) of Cl
5) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.40 Pain Relevance 0.20
Inflammatory mediators stimulate Cl- accumulation in DRGneurons
Positive_regulation (stimulate) of Positive_regulation (accumulation) of Cl associated with inflammatory mediators
6) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.54 Pain Relevance 0.52
They clearly demonstrate an increase of Cl- accumulation in reponse to inflammatory mediators, but they do not give information about which level of [Cl-]i is reached during the experiments.
Positive_regulation (increase) of Positive_regulation (accumulation) of Cl associated with inflammatory mediators
7) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.46 Pain Relevance 0.23
A number of similar observations have led to the concept that various forms of neurological disorders are associated with increased Cl- accumulation and with the resulting failure of GABAergic or glycinergic inhibition [8].
Positive_regulation (increased) of Positive_regulation (accumulation) of Cl associated with neurological disease and gabaergic
8) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.74 Pain Relevance 0.37
Cl- accumulation increases already after 2 hr (Fig. 2B) when the co-transporters are still at control level.
Positive_regulation (increases) of Positive_regulation (accumulation) of Cl
9) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.19 Pain Relevance 0.10
In line with this notion, our 2P-FLIM measurements suggest that inflammation boosts the excitatory potential of Cl- currents in DRG neurons through an increased efficiency of Cl- accumulation.


Positive_regulation (increased) of Positive_regulation (accumulation) of Cl in neurons associated with inflammation
10) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.70 Pain Relevance 0.35
These data demonstrate that the inflammatory mediators induce the phosphorylation of NKCC1 in DRG neurons and suggest that this phosphorylation causes the early (< 3 hr) phase of enhanced Cl- accumulation observed by 2P-FLIM in response to the stimulus.


Positive_regulation (enhanced) of Positive_regulation (accumulation) of Cl in neurons associated with inflammatory mediators
11) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.41 Pain Relevance 0.23

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