INT165011

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Context Info
Confidence 0.77
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 4.08
Pain Relevance 4.95

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

transport (SLC12A5) plasma membrane (SLC12A5) transmembrane transport (SLC12A5)
Anatomy Link Frequency
dendrites 1
horizontal cells 1
neuronal 1
spinal 1
spinal cord 1
SLC12A5 (Homo sapiens)
Pain Link Frequency Relevance Heat
Peripheral nerve injury 28 99.60 Very High Very High Very High
GABAergic 78 99.02 Very High Very High Very High
Neuropathic pain 146 98.96 Very High Very High Very High
gABA 98 97.20 Very High Very High Very High
Pain 60 96.56 Very High Very High Very High
Spinal cord 14 95.40 Very High Very High Very High
Glutamate receptor 14 91.92 High High
agonist 13 91.80 High High
allodynia 88 89.88 High High
hyperexcitability 70 88.72 High High
Disease Link Frequency Relevance Heat
Neuropathic Pain 306 99.92 Very High Very High Very High
Nervous System Injury 34 99.60 Very High Very High Very High
Ganglion Cysts 6 98.76 Very High Very High Very High
Pain 66 96.56 Very High Very High Very High
Inflammatory Pain 6 87.20 High High
Frailty 6 70.40 Quite High
Syndrome 12 59.52 Quite High
Myopia 44 59.44 Quite High
Epilepsy 13 51.52 Quite High
Disease 12 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Despite the decrease in KCC2 expression, spinal administration of benzodiazepines has been shown to be anti-allodynic in neuropathic conditions.
Gene_expression (expression) of KCC2 in spinal associated with neuropathic pain
1) Confidence 0.77 Published 2010 Journal Pain Section Abstract Doc Link 20007010 Disease Relevance 0.74 Pain Relevance 0.77
After peripheral nerve injury, a decrease in the expression of the K-Cl cotransporter KCC2, a major neuronal Cl(-) extruder, leads to pathologic alterations in GABA(A) and glycine receptor function in the spinal cord.
Gene_expression (expression) of KCC2 in spinal cord associated with gaba, nervous system injury, spinal cord and peripheral nerve injury
2) Confidence 0.77 Published 2010 Journal Pain Section Abstract Doc Link 20007010 Disease Relevance 0.32 Pain Relevance 0.55
In the developing brain GABAergic transmission is still excitatory due to reduced expression of the potassium chloride co-transporter 2 (KCC2) (Rivera et al., 1999).
Gene_expression (expression) of KCC2 in brain associated with gabaergic
3) Confidence 0.40 Published 2008 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2526001 Disease Relevance 0.05 Pain Relevance 0.29
KCC2 was also found to be expressed on the OFF bipolar dendrites, ganglion cell and bipolar axons whereas NKCC1 antibodies typically labelled horizontal cells as well as the ON bipolar dendrites [26].
Gene_expression (expressed) of KCC2 in horizontal cells associated with ganglion cysts
4) Confidence 0.34 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2481396 Disease Relevance 0.22 Pain Relevance 0.12
Thus KCC2 is expressed wherever the chloride equilibrium potential ECl<Erest (resting potential), whereas NKCC1 is expressed wherever ECl>Erest (ON bipolar dendrites).
Gene_expression (expressed) of KCC2 in dendrites
5) Confidence 0.34 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2481396 Disease Relevance 0.13 Pain Relevance 0.13
KCC2 expression or its direct effects on chloride extrusion from inside the cell, or upstream events including microglial activation and BDNF release [31,42]) but with no clinically available drugs to do this, other targets must be considered.
Gene_expression (expression) of KCC2
6) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0 Pain Relevance 0.16
In addition to reducing Eanion via decreased KCC2 expression, neuropathy leads to other pathophysiologic changes in lamina I and elsewhere in the pain pathway that undoubtedly contribute to the aberrant perception associated with neuropathic pain [1,3,77-79].
Gene_expression (expression) of KCC2 in lamina associated with pain and neuropathic pain
7) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.50 Pain Relevance 0.72
This could be explained by an increase in presynaptic inhibition, since primary afferent terminals do not express KCC2 and are therefore not prone to disinhibition by reduced KCC2 expression [31].
Gene_expression (expression) of KCC2
8) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.66 Pain Relevance 0.80
Additionally, we have not taken into account activity-dependent reduction of the chloride gradient [65-68], meaning a much smaller long-term reduction of Eanion (i.e. caused by reduced KCC2 expression) may cause incompensable disinhibition once dynamic, short-term reductions of Eanion (i.e. caused by activity-dependent reduction of the chloride gradient) are taken into account.
Gene_expression (expression) of KCC2
9) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.15 Pain Relevance 0.18
This could be explained by an increase in presynaptic inhibition, since primary afferent terminals do not express KCC2 and are therefore not prone to disinhibition by reduced KCC2 expression [31].
Neg (not) Gene_expression (express) of KCC2
10) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.63 Pain Relevance 0.77
The recent study by Coull et al. [31] suggests an alternative mechanism to explain disinhibition: reduced expression of the potassium-chloride cotransporter (KCC2) causes reduction of the chloride gradient across the neuronal membrane, which in turn leads to reduction of the anion reversal potential (i.e.
Gene_expression (expression) of KCC2 in neuronal
11) Confidence 0.11 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.67 Pain Relevance 0.47

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