INT121252

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Context Info
Confidence 0.61
First Reported 2004
Last Reported 2008
Negated 5
Speculated 0
Reported most in Body
Documents 10
Total Number 11
Disease Relevance 6.47
Pain Relevance 4.87

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

plasma membrane (Slc12a5) intracellular (Slc12a5) transmembrane transport (Slc12a5)
Anatomy Link Frequency
spinal cord 8
neurons 2
hippocampus 2
Slc12a5 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
long-term potentiation 10 100.00 Very High Very High Very High
Arthritis 5 99.84 Very High Very High Very High
Inflammatory mediators 138 99.20 Very High Very High Very High
Spinal cord 87 99.16 Very High Very High Very High
Hippocampus 23 98.72 Very High Very High Very High
Neuropathic pain 58 97.16 Very High Very High Very High
Hyperalgesia 78 96.40 Very High Very High Very High
IPN 1 94.56 High High
antagonist 23 93.72 High High
allodynia 21 92.96 High High
Disease Link Frequency Relevance Heat
Arthritis 5 99.84 Very High Very High Very High
INFLAMMATION 202 99.20 Very High Very High Very High
Spinal Cord Injury 216 98.32 Very High Very High Very High
Neuropathic Pain 94 97.16 Very High Very High Very High
Hyperalgesia 162 96.40 Very High Very High Very High
Inflammatory Pain 1 94.56 High High
Injury 40 91.68 High High
Contusions 12 85.52 High High
Ganglion Cysts 9 83.56 Quite High
Amnesia 1 83.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To explore a possible role of KCC2-dependent inhibition in anesthetic-induced impairment of LTP, we used field excitatory postsynaptic potentials (fEPSP) recording and immunoblotting to study the effect of propofol on LTP maintenance and KCC2 expression in CA1 region of rat hippocampal slices.
Regulation (effect) of Gene_expression (expression) of KCC2 associated with long-term potentiation
1) Confidence 0.61 Published 2006 Journal Brain Res. Bull. Section Abstract Doc Link 17027780 Disease Relevance 0.17 Pain Relevance 0.64
In accordance with these findings, estrogens failed to regulate KCC2 expression in the pyramidal region of the hippocampus of adult ovariectomized females, which likely have mature GABAAergic responses [218].


Neg (failed) Regulation (regulate) of Gene_expression (expression) of KCC2 in hippocampus associated with hippocampus
2) Confidence 0.45 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0 Pain Relevance 0.09
There were also no significant changes in KCC2 protein expression in rostral spinal cords on day 2–14 post-SCI (Figure 3B).


Neg (no) Regulation (changes) of Gene_expression (expression) of KCC2 protein in spinal cords associated with spinal cord injury
3) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 1.79 Pain Relevance 0.55
On the other hand, intraplantar formalin stimulation triggers a significant decrease in KCC2 protein expression without changes in NKCC1 in the rat spinal cord [18].
Neg (without) Regulation (changes) of Gene_expression (expression) of KCC2 protein in spinal cord associated with spinal cord
4) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 1.19 Pain Relevance 1.12
These data demonstrate that NKCC1 and KCC2 expression levels remain unchanged over 2 hr of treatment with inflammatory mediators.
Neg (unchanged) Regulation (unchanged) of Gene_expression (expression) of KCC2 associated with inflammatory mediators
5) Confidence 0.41 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.17 Pain Relevance 0.08
While the changes in NKCC1 and KCC2 expression are consistent with increased Cl- accumulation, the time course of the expression changes lags behind the rise in [Cl-]i.
Regulation (changes) of Gene_expression (expression) of KCC2
6) Confidence 0.41 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.15 Pain Relevance 0.08
Moreover, transient increase in NKCC1 protein and down-regulation of KCC2 expression were detected in the spinal cord following SCI.
Regulation (regulation) of Gene_expression (expression) of KCC2 in spinal cord associated with spinal cord injury and spinal cord
7) Confidence 0.26 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 1.51 Pain Relevance 0.84
Our objective was to monitor changes of the intracellular Cl- concentration as well as changes in expression of NKCC1 and KCC2 in the presence of inflammatory mediators.
Regulation (changes) of Gene_expression (expression) of KCC2 associated with inflammatory mediators
8) Confidence 0.25 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.55 Pain Relevance 0.43
For instance, in male infantile (PN15) SN neurons, GABAAergic depolarizations increase intracellular calcium, the expression of the phosphorylated form of the transcriptional factor CREB (cAMP responsive element binding protein), as well as the expression of calcium regulated mRNAs, such as KCC2 [79, 80, 82].
Regulation (regulated) of Gene_expression (expression) of KCC2 in neurons
9) Confidence 0.20 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0 Pain Relevance 0.11
Altered KCC2 and NKCC1 expression in arthritis may contribute to the control of spinal cord excitability and may represent novel therapeutic targets in the treatment of inflammatory pain.
Regulation (Altered) of Gene_expression (expression) of KCC2 in spinal cord associated with ipn, spinal cord and arthritis
10) Confidence 0.15 Published 2004 Journal Neurobiol. Dis. Section Abstract Doc Link 15350966 Disease Relevance 0.93 Pain Relevance 0.83
The KCl-induced change in ECl did not correspond with alterations in the expression of the cation chloride cotransporters KCC2 and NKCC1, as determined by western blotting (p=0.736).
Neg (not) Regulation (alterations) of Gene_expression (expression) of KCC2
11) Confidence 0.07 Published 2008 Journal Brain Res. Section Abstract Doc Link 18353290 Disease Relevance 0 Pain Relevance 0.12

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