INT165013

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Context Info
Confidence 0.58
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 7
Disease Relevance 3.55
Pain Relevance 4.22

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
lamina 4
neuronal 2
spinal 2
spinal cord 2
SLC12A5 (Homo sapiens)
Pain Link Frequency Relevance Heat
Peripheral nerve injury 24 99.92 Very High Very High Very High
Neuropathic pain 123 99.44 Very High Very High Very High
GABAergic 52 97.60 Very High Very High Very High
gABA 81 97.20 Very High Very High Very High
Pain 50 96.56 Very High Very High Very High
Spinal cord 12 95.40 Very High Very High Very High
agonist 10 89.36 High High
IPN 5 87.60 High High
allodynia 74 87.44 High High
Dorsal horn neuron 2 84.64 Quite High
Disease Link Frequency Relevance Heat
Neuropathic Pain 258 99.92 Very High Very High Very High
Nervous System Injury 29 99.92 Very High Very High Very High
Pain 55 96.56 Very High Very High Very High
Inflammatory Pain 5 87.60 High High
Frailty 5 70.40 Quite High
Syndrome 10 59.84 Quite High
Urological Neuroanatomy 5 49.28 Quite Low
Hyperalgesia 55 47.36 Quite Low
Disease 5 45.56 Quite Low
Nociception 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
Negative_regulation (decrease) of Gene_expression (expression) of KCC2 in spinal cord associated with gaba, nervous system injury, spinal cord and peripheral nerve injury
1) Confidence 0.58 Published 2010 Journal Pain Section Abstract Doc Link 20007010 Disease Relevance 0.32 Pain Relevance 0.55
Despite the decrease in KCC2 expression, spinal administration of benzodiazepines has been shown to be anti-allodynic in neuropathic conditions.
Negative_regulation (decrease) of Gene_expression (expression) of KCC2 in spinal associated with neuropathic pain
2) Confidence 0.58 Published 2010 Journal Pain Section Abstract Doc Link 20007010 Disease Relevance 0.74 Pain Relevance 0.77
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].
Negative_regulation (reduced) of Gene_expression (expression) of KCC2
3) Confidence 0.11 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.66 Pain Relevance 0.80
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].
Negative_regulation (decreased) of Gene_expression (expression) of KCC2 in lamina associated with pain and neuropathic pain
4) Confidence 0.11 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.50 Pain Relevance 0.73
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.
Negative_regulation (reduced) of Gene_expression (expression) of KCC2 in neuronal
5) Confidence 0.08 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.68 Pain Relevance 0.47
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.
Negative_regulation (reduced) of Gene_expression (expression) of KCC2
6) Confidence 0.08 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.15 Pain Relevance 0.18
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].
Negative_regulation (decreased) of Gene_expression (expression) of KCC2 in lamina associated with pain and neuropathic pain
7) Confidence 0.08 Published 2006 Journal Mol Pain Section Body Doc Link PMC1624821 Disease Relevance 0.50 Pain Relevance 0.73

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