INT138890

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Context Info
Confidence 0.45
First Reported 2006
Last Reported 2008
Negated 3
Speculated 4
Reported most in Body
Documents 12
Total Number 21
Disease Relevance 11.61
Pain Relevance 7.46

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
neurons 4
spinal cord 2
neuronal 1
spinal 1
dentate gyrus 1
Slc12a5 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
bDMF 70 99.84 Very High Very High Very High
Hippocampus 77 99.74 Very High Very High Very High
Inflammatory mediators 138 99.68 Very High Very High Very High
Neuropathic pain 136 99.48 Very High Very High Very High
Sciatic nerve 9 99.44 Very High Very High Very High
spinal dorsal horn 12 99.28 Very High Very High Very High
Pain 44 99.20 Very High Very High Very High
gABA 392 98.96 Very High Very High Very High
Spinal cord 193 98.72 Very High Very High Very High
Hyperalgesia 139 98.72 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 206 99.68 Very High Very High Very High
Spinal Cord Injury 504 99.48 Very High Very High Very High
Neuropathic Pain 216 99.48 Very High Very High Very High
Contusions 28 99.40 Very High Very High Very High
Pain 45 99.20 Very High Very High Very High
Nervous System Injury 92 98.96 Very High Very High Very High
Hyperalgesia 335 98.72 Very High Very High Very High
Convulsion 210 96.48 Very High Very High Very High
Nociception 86 95.80 Very High Very High Very High
Injury 105 95.24 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Given the divergent patterns of regulation of KCC2 in neurons with depolarizing vs hyperpolarizing GABAAergic signaling (Fig. 2), can these observations be extended to neonatal and pediatric epilepsies, when the brain is still immature?
Regulation (regulation) of KCC2 in neurons associated with epilepsy
1) Confidence 0.45 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0.73 Pain Relevance 0.19
The sexually dimorphic features of the PN15 rat SNR have provided us with a convenient in vivo system to study KCC2 regulation in normal neurons with similar chronological age, which have either depolarizing (male) or hyperpolarizing (female) GABAAergic signaling.
Regulation (regulation) of KCC2 in neurons
2) Confidence 0.45 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0 Pain Relevance 0.32
A number of studies have also investigated the regulation of KCC2 and GABAAergic switch by GABA signaling, showing that depolarizing GABAAergic signaling is a positive drive for the developmental upregulation of KCC2 and switch of GABAA receptors, mediating its effects through activation of voltage-sensitive calcium channels and activation of calcium signaling.
Spec (investigated) Regulation (regulation) of KCC2 associated with gaba and calcium channel
3) Confidence 0.45 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0 Pain Relevance 0.16
To further establish that changes in NKCC1 and KCC2 are specific to the lesion epicenter of the spinal cord in response to SCI, we also examined spinal cord tissue rostral to the SCI injury epicenter.
Regulation (specific) of KCC2 in spinal cord associated with spinal cord injury, injury and spinal cord
4) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 1.57 Pain Relevance 0.35
A recent report shows that this transient down-regulation of KCC2 [22] and the early pain behavior depends on activation of TrkB receptor via BDNF in nerve injury [12].
Regulation (regulation) of KCC2 in nerve associated with pain and nervous system injury
5) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 0.71 Pain Relevance 0.34
The significance of changes of NKCC1 and KCC2 proteins following SCI is not clear.
Regulation (changes) of KCC2 associated with spinal cord injury
6) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 0.79 Pain Relevance 0.34
We examined changes in NKCC1 and KCC2 protein levels in the contusion epicenter of spinal cord during days 21–42 post-SCI, when it was possible to determine the presence of chronic TH.
Spec (examined) Regulation (changes) of KCC2 protein in spinal cord associated with spinal cord injury, thermal hyperalgesia, contusions and spinal cord
7) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 1.88 Pain Relevance 0.57
Post-translational modulation of KCC2 appears to be involved in the down-regulation of KCC2 protein.
Regulation (regulation) of KCC2 protein
8) Confidence 0.43 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 0.72 Pain Relevance 0.24
The activity of NKCC1 and KCC2 can be modulated by phosphorylation [26,27].
Regulation (modulated) of KCC2
9) Confidence 0.41 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.17 Pain Relevance 0.09
These data demonstrate that NKCC1 and KCC2 expression levels remain unchanged over 2 hr of treatment with inflammatory mediators.
Neg (unchanged) Regulation (unchanged) of KCC2 associated with inflammatory mediators
10) Confidence 0.41 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.17 Pain Relevance 0.08
Amygdalar kindling of adult rats increased NKCC1 in the piriform cortex [231] and dentate gyrus [232]; decreased KCC1 and Clc2 in the dentate gyrus and Clc2 in the CA1 pyramidal region of the hippocampus, but had no effect on KCC2 [232].
Neg (no) Regulation (effect) of KCC2 in dentate gyrus associated with hippocampus
11) Confidence 0.39 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0.60 Pain Relevance 0.24
The developmental and cell type specific expression of these signaling pathways may be therefore important in the developmental regulation of KCC2 by BDNF.
Regulation (regulation) of KCC2 associated with bdmf
12) Confidence 0.33 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0.07 Pain Relevance 0.38
On a separate note, Ludwig et al. did not observe any changes in KCC2 immunoreactivity in cultured PN0-1 hippocampal mouse neurons chronically treated with either picrotoxin and the sodium channel inhibitor tetrodotoxin (TTX) or combinations of TTX with glutamate receptor inhibitors, proposing that these are not necessary for the developmental increase in KCC2, in hippocampus [180].
Neg (not) Regulation (changes) of KCC2 in neurons associated with tetrodotoxin, glutamate receptor, sodium channel and hippocampus
13) Confidence 0.33 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0 Pain Relevance 0.64
We, therefore, investigated expression changes of KCC2 and NKCC1 in the spinal dorsal horn of the rat after the intraplantar injection of formalin as an acute nociceptive stimulus.
Spec (investigated) Regulation (changes) of KCC2 in spinal associated with nociception and spinal dorsal horn
14) Confidence 0.27 Published 2006 Journal Neurosci. Res. Section Abstract Doc Link 17007947 Disease Relevance 0.65 Pain Relevance 0.70
Changes of K+ -Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices.
Regulation (Changes) of KCC2 associated with long-term potentiation
15) Confidence 0.27 Published 2006 Journal Brain Res. Bull. Section Title Doc Link 17027780 Disease Relevance 0.17 Pain Relevance 0.48
Changes of K+ -Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices.
Regulation (Changes) of K+ -Cl- cotransporter 2 associated with long-term potentiation
16) Confidence 0.27 Published 2006 Journal Brain Res. Bull. Section Title Doc Link 17027780 Disease Relevance 0.17 Pain Relevance 0.48
Post-translational modulation of KCC2 appears to be involved in the down-regulation of KCC2 protein.
Regulation (modulation) of KCC2
17) Confidence 0.26 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 0.68 Pain Relevance 0.25
In summary, we investigated the roles of two major intracellular Cl- regulatory proteins, NKCC1 and KCC2, in chronic neuropathic pain following contusive SCI in the rat model.
Spec (investigated) Regulation (roles) of KCC2 associated with spinal cord injury and neuropathic pain
18) Confidence 0.26 Published 2008 Journal Mol Pain Section Body Doc Link PMC2561007 Disease Relevance 1.14 Pain Relevance 0.63
Coull et al. (2003) proposed that sciatic nerve constriction led to a down-regulation of the potassium-chloride transporter KCC2 in lamina I neurons, which meant that IPSCs could be depolarizing, thus increasing the excitatory drive to these neurons and contributing to neuropathic symptoms.
Regulation (regulation) of KCC2 in sciatic nerve associated with neuropathic pain and sciatic nerve
19) Confidence 0.25 Published 2008 Journal Neuroscience Section Body Doc Link PMC2553186 Disease Relevance 0.68 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 KCC2 in neurons
20) Confidence 0.20 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645547 Disease Relevance 0 Pain Relevance 0.11

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