INT23331

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Context Info
Confidence 0.54
First Reported 1985
Last Reported 2010
Negated 0
Speculated 3
Reported most in Abstract
Documents 10
Total Number 13
Disease Relevance 4.63
Pain Relevance 8.76

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

extracellular space (Tac1) extracellular region (Tac1) plasma membrane (Tac1)
Anatomy Link Frequency
cholinergic neurons 4
dorsal root ganglion 2
dorsal horn 2
Tac1 (Mus musculus)
Pain Link Frequency Relevance Heat
substance P 109 100.00 Very High Very High Very High
Glutamate 19 100.00 Very High Very High Very High
Neuropeptide 9 100.00 Very High Very High Very High
qutenza 219 99.98 Very High Very High Very High
primary afferent fibers 20 99.98 Very High Very High Very High
calcitonin gene related peptide 28 99.90 Very High Very High Very High
Opioid 1 99.84 Very High Very High Very High
vaginimus 5 99.52 Very High Very High Very High
dorsal root ganglion 7 99.20 Very High Very High Very High
antagonist 93 98.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Dyspareunia 5 99.52 Very High Very High Very High
Nociception 53 99.44 Very High Very High Very High
Increased Venous Pressure Under Development 13 99.00 Very High Very High Very High
Ganglion Cysts 12 98.72 Very High Very High Very High
Neurogenic Inflammation 3 96.96 Very High Very High Very High
INFLAMMATION 61 93.72 High High
Syndrome 1 93.52 High High
Pain 86 93.12 High High
Malignant Neoplastic Disease 2 92.28 High High
Hematological Disease 12 91.88 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Leukotriene D4 did not cause synaptic transmitter release through ganglionic stimulation, because its contractile effect was tetrodotoxin insensitive, and did not contribute to noncholinergic excitation through stimulation of neurokinin A release, as the neurokinin2 receptor antagonist, MEN 10,376, did not alter the response to leukotriene D4.
Positive_regulation (stimulation) of Localization (release) of neurokinin associated with tetrodotoxin and antagonist
1) Confidence 0.54 Published 1995 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7616450 Disease Relevance 0.14 Pain Relevance 0.34
Capsaicin induces the release of substance P (SP) by PAFs, producing vasodilation and increasing vascular permeability (neurogenic inflammation).
Positive_regulation (induces) of Localization (release) of substance P associated with inflammation, qutenza, primary afferent fibers, neurogenic inflammation, increased venous pressure under development and substance p
2) Confidence 0.38 Published 1995 Journal J Reprod Med Section Abstract Doc Link 7608871 Disease Relevance 1.08 Pain Relevance 1.27
This propagation was suppressed by 5 microM L-703.606, an NK1-receptor antagonist, suggesting that the repetitive stimulation-elicited excitation may require substance-P releases.
Spec (may) Positive_regulation (require) of Localization (releases) of substance-P associated with antagonist
3) Confidence 0.37 Published 2005 Journal Neurosci. Res. Section Abstract Doc Link 15927721 Disease Relevance 0.15 Pain Relevance 0.23
This suggests that stimulation by capsaicin of TRPV1 receptors on primary afferent fibres causes a release of tachykinins which, in turn, mediate via NK1 and NK3 receptors an increase in acetylcholine release.
Positive_regulation (causes) of Localization (release) of NK1 associated with qutenza and primary afferent fibers
4) Confidence 0.32 Published 2006 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 16328494 Disease Relevance 0 Pain Relevance 0.76
The facilitatory effect is indirect and involves tachykinin release and excitation of NK1 and NK3 receptors on cholinergic neurons.
Positive_regulation (excitation) of Localization (release) of NK1 in cholinergic neurons
5) Confidence 0.32 Published 2006 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 16328494 Disease Relevance 0 Pain Relevance 0.64
The facilitatory effect is indirect and involves tachykinin release and excitation of NK1 and NK3 receptors on cholinergic neurons.
Positive_regulation (involves) of Localization (release) of NK1 in cholinergic neurons
6) Confidence 0.32 Published 2006 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 16328494 Disease Relevance 0 Pain Relevance 0.64
This suggests that stimulation by capsaicin of TRPV1 receptors on primary afferent fibres causes a release of tachykinins which, in turn, mediate via NK1 and NK3 receptors an increase in acetylcholine release.
Positive_regulation (increase) of Localization (release) of NK1 associated with qutenza and primary afferent fibers
7) Confidence 0.32 Published 2006 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 16328494 Disease Relevance 0 Pain Relevance 0.77
This study was conducted to determine whether Na(v)1.8 contributes to the release and/or synthesis of substance P (SP) in adult mice dorsal root ganglion (DRG) neurons.
Spec (whether) Positive_regulation (contributes) of Localization (release) of substance P in dorsal root ganglion associated with ganglion cysts, dorsal root ganglion and substance p
8) Confidence 0.22 Published 2008 Journal J. Pharmacol. Sci. Section Abstract Doc Link 18845912 Disease Relevance 0.86 Pain Relevance 0.71
It excites nociceptive primary afferent fibers to release glutamate and neuropeptides including substance P through activation of TRPV1 receptors [13-15].
Positive_regulation (activation) of Localization (release) of substance P associated with nociception, glutamate, primary afferent fibers, neuropeptide and substance p
9) Confidence 0.12 Published 2005 Journal Mol Pain Section Body Doc Link PMC1185563 Disease Relevance 0.20 Pain Relevance 1.02
This effect is TRPV1 specific as it was inhibited by capsazepine and suggested to occur as a result of CGRP and tachykinin release upon TRPV1 activation [86].
Positive_regulation (upon) of Localization (release) of tachykinin associated with calcitonin gene related peptide
10) Confidence 0.03 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.64 Pain Relevance 0.55
This effect is TRPV1 specific as it was inhibited by capsazepine and suggested to occur as a result of CGRP and tachykinin release upon TRPV1 activation [86].
Positive_regulation (activation) of Localization (release) of tachykinin associated with calcitonin gene related peptide
11) Confidence 0.03 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.65 Pain Relevance 0.56
Increased expression or release of Substance-P following neurotrophic stimulation of cells has been described in diverse settings documenting its important role in the hematopoietic-neuro-immune axis in inflammation, as well as normal and malignant hematopoiesis[57]–[62].
Positive_regulation (Increased) of Localization (release) of Substance-P associated with hematological disease, malignant neoplastic disease and inflammation
12) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2837737 Disease Relevance 0.91 Pain Relevance 0.28
The effects of locally applied opioids on the release of immunoreactive Substance P (iSP), induced by mechanical stimuli, from the dorsal horn of the rabbit in situ, were investigated.
Spec (investigated) Positive_regulation (induced) of Localization (release) of immunoreactive Substance P in dorsal horn associated with dorsal horn, opioid and substance p
13) Confidence 0.02 Published 1985 Journal Neuropharmacology Section Abstract Doc Link 2410807 Disease Relevance 0 Pain Relevance 0.98

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