INT41487

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Context Info
Confidence 0.57
First Reported 1984
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 27
Disease Relevance 9.42
Pain Relevance 25.20

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 3
neurons 1
nerve 1
adrenal medulla 1
posterior 1
Cacna1a (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 1607 100.00 Very High Very High Very High
qutenza 955 100.00 Very High Very High Very High
Glutamate 64 100.00 Very High Very High Very High
Migraine 56 100.00 Very High Very High Very High
tetrodotoxin 54 100.00 Very High Very High Very High
long-term potentiation 888 99.96 Very High Very High Very High
Calcium channel 18 99.96 Very High Very High Very High
narcan 21 99.84 Very High Very High Very High
Calcitonin gene-related peptide 24 99.24 Very High Very High Very High
medulla 14 99.24 Very High Very High Very High
Disease Link Frequency Relevance Heat
Migraine With Aura 29 100.00 Very High Very High Very High
Epilepsy 14 99.48 Very High Very High Very High
INFLAMMATION 129 98.84 Very High Very High Very High
Neurological Disease 2 98.32 Very High Very High Very High
Headache 27 96.40 Very High Very High Very High
Targeted Disruption 113 95.96 Very High Very High Very High
Hypertrophy 2 94.88 High High
Diabetes Mellitus 8 94.64 High High
Ataxia 4 93.56 High High
Spinocerebellar Ataxia Type 2 2 91.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We observed that caffeic acid could enhance BER release from isolated rat adrenal medulla in a concentration-dependent manner; inhibitors of alpha 1A -adrenoceptors such as WB 4101 and RS 1705 abolished this action.
Negative_regulation (inhibitors) of alpha 1A in adrenal medulla associated with medulla
1) Confidence 0.57 Published 2003 Journal Horm. Metab. Res. Section Abstract Doc Link 12778369 Disease Relevance 0.55 Pain Relevance 0.39
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).
Negative_regulation (decreased) of FHM3 in brain associated with glutamate and migraine
2) Confidence 0.43 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.83 Pain Relevance 1.00
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).
Negative_regulation (decreased) of FHM1 in brain associated with glutamate and migraine
3) Confidence 0.43 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.80 Pain Relevance 0.96
This identification of an intrinsic defect in FHM1 mutant channels helps explain their impact on neurotransmission when they occupy type-specific slots for P/Q channels at central nerve terminals.
Negative_regulation (defect) of FHM1 in nerve
4) Confidence 0.42 Published 2005 Journal J. Biol. Chem. Section Abstract Doc Link 15795222 Disease Relevance 0.07 Pain Relevance 0.16
Knockdown of Cav2.1 calcium channels is sufficient to induce neurological disorders observed in natural occurring Cacna1a mutants in mice.
Negative_regulation (Knockdown) of Cav2.1 associated with neurological disease and calcium channel
5) Confidence 0.42 Published 2009 Journal Biochem. Biophys. Res. Commun. Section Title Doc Link 19854154 Disease Relevance 0.88 Pain Relevance 0.21
Mutations in three genes have been described in FHM patients: CACNA1A (FHM1), ATP1A2 (FHM2) and SCN1A (FHM3).
Negative_regulation (described) of FHM1 associated with migraine
6) Confidence 0.25 Published 2008 Journal Cephalalgia Section Abstract Doc Link 18644040 Disease Relevance 1.26 Pain Relevance 0.89
Mutations in three genes have been described in FHM patients: CACNA1A (FHM1), ATP1A2 (FHM2) and SCN1A (FHM3).
Negative_regulation (described) of CACNA1A associated with migraine
7) Confidence 0.25 Published 2008 Journal Cephalalgia Section Abstract Doc Link 18644040 Disease Relevance 1.25 Pain Relevance 0.89
As described above, partial inhibition of TTX-R currents in Tg-t-MrVIa was observed with no evidence of compensation by TTX-S currents.
Negative_regulation (inhibition) of Tg-t-MrVIa associated with tetrodotoxin
8) Confidence 0.18 Published 2010 Journal The Journal of Physiology Section Body Doc Link PMC2887988 Disease Relevance 0.25 Pain Relevance 1.54
Together with the strong decrease in Cortico-LA PPR in adult Mecp2308/Y mice (Fig. 2), we conclude that the prolonged absence of Mecp2 strongly increased release probability at Cortico-LA synapses, possibly compensating for the progressive synaptic elimination.


Negative_regulation (decrease) of LA in synapses associated with amygdala
9) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0 Pain Relevance 0.47
Detection of a novel missense mutation and second recurrent mutation in the CACNA1A gene in individuals with EA-2 and FHM.
Negative_regulation (Detection) of FHM
10) Confidence 0.11 Published 1999 Journal Hum. Genet. Section Title Doc Link 10987655 Disease Relevance 0.51 Pain Relevance 0.32
The results of this study indicate that the selectivity of alpha-1 or alpha-2 receptor blockade in mice and rats can be reliably determined by using behavioral parameters.
Negative_regulation (blockade) of alpha-1
11) Confidence 0.09 Published 1984 Journal Pol J Pharmacol Pharm Section Abstract Doc Link 6152494 Disease Relevance 0 Pain Relevance 0.28
Our results indicate that the effect of antecedent ethanol ingestion to prevent postischemic LR and LA is initiated by a CGRP-dependent mechanism.
Negative_regulation (prevent) of LA associated with calcitonin gene-related peptide
12) Confidence 0.07 Published 2006 Journal Am. J. Physiol. Heart Circ. Physiol. Section Abstract Doc Link 16143644 Disease Relevance 0.32 Pain Relevance 1.03
This release of cannabinoids seems to be responsible for the capsaicin-evoked suppression of LA-LTP.
Negative_regulation (suppression) of LA associated with qutenza, cannabinoid, long-term potentiation and amygdala
13) Confidence 0.06 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 0.98
Our results suggest that GABAB receptors are not involved in mediating capsaicin-induced suppression of LA-LTP.
Negative_regulation (suppression) of LA associated with qutenza, long-term potentiation and amygdala
14) Confidence 0.06 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0.18 Pain Relevance 1.61
L-NAME pretreatment clearly reduced the magnitude of LA-LTP; however, the co-application of L-NAME and capsaicin blocked the capsaicin-induced reduction of LA-LTP.
Negative_regulation (reduction) of LA associated with qutenza, long-term potentiation and amygdala
15) Confidence 0.06 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0.08 Pain Relevance 1.59
Capsaicin dose-dependently reduces LA-LTP in horizontal slices
Negative_regulation (reduces) of LA associated with qutenza, long-term potentiation and amygdala
16) Confidence 0.04 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.08
The specific antagonist of cannabinoid receptor type 1 (CB1), AM 251, was also able to reduce the inhibitory effect of capsaicin on LA-LTP, suggesting that stimulation of TRPV1 provokes the generation of anandamide in the brain which seems to inhibit NO synthesis.
Negative_regulation (reduce) of LA in brain associated with qutenza, cannabinoid receptor, antagonist, long-term potentiation and amygdala
17) Confidence 0.04 Published 2011 Journal PLoS ONE Section Abstract Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.62
The capsaicin-induced reduction of LA-LTP could be also blocked by the specific TRPV1 antagonist AMG9810 (1 µM cap: 110.4±5.5% [n?
Negative_regulation (reduction) of LA associated with qutenza, antagonist, long-term potentiation and amygdala
18) Confidence 0.04 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.76
Our results further show that capsaicin-induced suppression of HFS-induced LA-LTP is mediated by the stimulation of TRPV1 receptors, since capsazepine and AMG9810 blocked the capsaicin-induced effect and the effect was absent in TRPV1 deficient mice.
Negative_regulation (suppression) of LA associated with qutenza, long-term potentiation and amygdala
19) Confidence 0.04 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0.32 Pain Relevance 1.62
This co-application also did not block the suppressive action of capsaicin on LA-LTP (SR: 130.2±6.0% [n?
Negative_regulation (block) of LA associated with qutenza, long-term potentiation and amygdala
20) Confidence 0.04 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 0.89

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