INT71629

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Context Info
Confidence 0.15
First Reported 1997
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 7
Disease Relevance 1.42
Pain Relevance 1.10

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

Anatomy Link Frequency
spike 3
Swd1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Action potential 43 99.64 Very High Very High Very High
Dopamine 186 93.36 High High
Thalamus 52 90.24 High High
tetrodotoxin 6 89.52 High High
cerebral cortex 18 77.36 Quite High
sodium channel 4 64.48 Quite High
Pyramidal cell 5 63.68 Quite High
Glutamate receptor 16 61.92 Quite High
potassium channel 6 56.88 Quite High
Neuronal excitability 4 54.16 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 36 95.76 Very High Very High Very High
Convulsion 20 86.00 High High
Congenital Anomalies 8 84.08 Quite High
Absence Epilepsy 60 81.36 Quite High
Sprains And Strains 80 79.88 Quite High
Generalized Epilepsy 8 58.72 Quite High
Unconsciousness 4 8.16 Low Low
Ataxia 20 5.00 Very Low Very Low Very Low
Parkinson's Disease 10 5.00 Very Low Very Low Very Low
Epilepsy 9 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A high-threshold Ca(2+)-conductance was also found to contribute to the action potential as judged by the decrease in spike duration towards the peak observed during Ca(2+)-conductance block.
Negative_regulation (decrease) of spike in spike associated with action potential
1) Confidence 0.15 Published 1997 Journal Neuroscience Section Abstract Doc Link 9330357 Disease Relevance 0 Pain Relevance 0.34
As shown for the Gria4spkw1 allele previously, the SWD of homozygous Gria4tm1Dgen mice coincide with an arrest of normal behavior and are suppressed by treatment with the anti-absence drug ethosuximide (Fig. 4B).
Negative_regulation (suppressed) of SWD
2) Confidence 0.01 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.13 Pain Relevance 0
The physiological mechanism leading to SWD in these mutants is not yet clear, although several mutants have an accompanying up-regulation of T-type Ca2+ channel activity (13), and in the presence of the Cacna1g mutation the high-threshold VDCC mutants have reduced SWD (14), suggesting a possible means of generating SWD by increasing Ca2+-dependent burst firing—supported by the analysis of human mutations in T-type VDCC genes (reviewed in 6).
Negative_regulation (reduced) of SWD
3) Confidence 0.01 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.50 Pain Relevance 0.06
To confirm the causal relationship between Gria4 deficiency and SWD, we assessed the electroencephalographic phenotype of an independent mutation of Gria4: the Gria4tm1Dgen knockout allele (expression defect data are shown in Figure 3B and C; see Materials and Methods for more details on the origin and nature of Gria4tm1Dgen).
Negative_regulation (deficiency) of SWD associated with targeted disruption
4) Confidence 0.01 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.22 Pain Relevance 0
In contrast, null mutants for the related gene Gria3 do not have SWD, and Gria3 loss actually lowers SWD of spkw1 homozygotes.
Negative_regulation (loss) of SWD
5) Confidence 0.00 Published 2008 Journal Human Molecular Genetics Section Abstract Doc Link PMC2405903 Disease Relevance 0.56 Pain Relevance 0.12
In these conditions, we showed a decrease in the rheobase current, a decrease in the latency to the first spike, a leftward shift of the current – firing frequency plot, a decrease in the spike threshold and an increase in the slope of the ramp potential evoked by a subthreshold depolarizing current pulse.
Negative_regulation (decrease) of spike in spike
6) Confidence 0.00 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2733153 Disease Relevance 0 Pain Relevance 0.26
In these conditions, we showed a decrease in the rheobase current, a decrease in the latency to the first spike, a leftward shift of the current – firing frequency plot, a decrease in the spike threshold and an increase in the slope of the ramp potential evoked by a subthreshold depolarizing current pulse.
Negative_regulation (decrease) of spike in spike
7) Confidence 0.00 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2733153 Disease Relevance 0 Pain Relevance 0.31

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