INT142940

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Context Info
Confidence 0.50
First Reported 2007
Last Reported 2011
Negated 0
Speculated 0
Reported most in Abstract
Documents 3
Total Number 3
Disease Relevance 1.65
Pain Relevance 2.97

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

transport (Cacna1a) DNA binding (Cacna1a) transmembrane transport (Cacna1a)
cytoplasm (Cacna1a) cell death (Cacna1a) nucleus (Cacna1a)
Anatomy Link Frequency
brain 4
Cacna1a (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 126 100.00 Very High Very High Very High
qutenza 79 100.00 Very High Very High Very High
Glutamate 9 100.00 Very High Very High Very High
long-term potentiation 74 99.96 Very High Very High Very High
Cannabinoid 7 99.74 Very High Very High Very High
Migraine 22 99.44 Very High Very High Very High
Hippocampus 6 96.08 Very High Very High Very High
hyperexcitability 4 92.88 High High
depression 5 84.92 Quite High
GABAergic 9 83.04 Quite High
Disease Link Frequency Relevance Heat
Migraine With Aura 14 99.44 Very High Very High Very High
Headache 8 96.40 Very High Very High Very High
Epilepsy 3 86.76 High High
Depression 5 84.92 Quite High
Pain 5 32.76 Quite Low
Targeted Disruption 2 16.92 Low Low
Anxiety Disorder 7 5.00 Very Low Very Low Very Low
Nociception 2 5.00 Very Low Very Low Very Low
Hyperalgesia 1 5.00 Very Low Very Low Very Low
Drug Induced Neurotoxicity 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These findings are consistent with the hypothesis that FHM mutations share the ability of rendering the brain more susceptible to CSD by causing either excessive synaptic glutamate release (FHM1) or decreased removal of K+ and glutamate from the synaptic cleft (FHM2) or excessive extracellular K+ (FHM3).
Positive_regulation (causing) of Negative_regulation (decreased) of FHM3 in brain associated with glutamate and migraine
1) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.84 Pain Relevance 1.01
These findings are consistent with the hypothesis that FHM mutations share the ability of rendering the brain more susceptible to CSD by causing either excessive synaptic glutamate release (FHM1) or decreased removal of K+ and glutamate from the synaptic cleft (FHM2) or excessive extracellular K+ (FHM3).
Positive_regulation (causing) of Negative_regulation (decreased) of FHM1 in brain associated with glutamate and migraine
2) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.82 Pain Relevance 0.97
This release of cannabinoids seems to be responsible for the capsaicin-evoked suppression of LA-LTP.
Positive_regulation (responsible) of Negative_regulation (suppression) of LA associated with qutenza, cannabinoid, long-term potentiation and amygdala
3) Confidence 0.05 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 0.98

General Comments

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