INT8690

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Context Info
Confidence 0.80
First Reported 1983
Last Reported 2010
Negated 0
Speculated 1
Reported most in Abstract
Documents 71
Total Number 72
Disease Relevance 22.98
Pain Relevance 50.75

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
spinal cord 7
sensory nerves 6
nerve 6
dorsal horn 3
smooth muscle 2
Tac1 (Mus musculus)
Pain Link Frequency Relevance Heat
substance P 830 100.00 Very High Very High Very High
qutenza 307 100.00 Very High Very High Very High
Inflammation 266 100.00 Very High Very High Very High
Glutamate 92 100.00 Very High Very High Very High
primary afferent fibers 72 100.00 Very High Very High Very High
Calcitonin gene-related peptide 45 100.00 Very High Very High Very High
Neuropeptide 42 100.00 Very High Very High Very High
Enkephalin 39 100.00 Very High Very High Very High
Somatostatin 36 100.00 Very High Very High Very High
dorsal root ganglion 24 100.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 276 100.00 Very High Very High Very High
Ganglion Cysts 30 100.00 Very High Very High Very High
Neurogenic Inflammation 21 100.00 Very High Very High Very High
Generalized Anxiety Disorder 7 100.00 Very High Very High Very High
Nociception 128 99.76 Very High Very High Very High
Pain 122 99.68 Very High Very High Very High
Targeted Disruption 53 99.60 Very High Very High Very High
Stress 4 99.50 Very High Very High Very High
Rheumatoid Arthritis 30 99.28 Very High Very High Very High
Cough 6 99.26 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Basal and activity-induced release of substance P from primary afferent fibres in NK1 receptor knockout mice: evidence for negative feedback.
Localization (release) of NK1 associated with targeted disruption, qutenza, primary afferent fibers and substance p
1) Confidence 0.80 Published 2003 Journal Neuropharmacology Section Title Doc Link 14614953 Disease Relevance 0.31 Pain Relevance 0.74
SP release was assayed in the mouse stomach, ROS were detected using dichlorofluorescein diacetate, and neurokinin 1 receptors were localized by immunofluorescence.
Localization (localized) of neurokinin 1 in stomach associated with substance p
2) Confidence 0.73 Published 2007 Journal Free Radic. Biol. Med. Section Abstract Doc Link 17640568 Disease Relevance 0.07 Pain Relevance 0.52
The depressor response induced by rat/mouse hemokinin-1 (i.v.) might be explained primarily by the action on endothelial tachykinin NK1 receptors to release endothelium-derived relaxing factor (NO) and this effect was not affected by vagal components.
Localization (release) of tachykinin in endothelium
3) Confidence 0.73 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17628523 Disease Relevance 0 Pain Relevance 0.28
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.
Localization (release) of neurokinin associated with tetrodotoxin and antagonist
4) Confidence 0.63 Published 1995 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7616450 Disease Relevance 0.14 Pain Relevance 0.34
Instead leukotriene D4 may modulate the release of neurokinin A from nerve endings during nerve stimulation.
Localization (release) of neurokinin in nerve
5) Confidence 0.63 Published 1995 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7616450 Disease Relevance 0.13 Pain Relevance 0.32
Neurogenic inflammation, which results from peripheral release of substance P and neurokinin A, is almost absent in the mutant mice.
Localization (release) of neurokinin associated with inflammation, neurogenic inflammation and substance p
6) Confidence 0.62 Published 1998 Journal Nature Section Abstract Doc Link 9537322 Disease Relevance 0.43 Pain Relevance 1.19
Morphine inhibits substance P release from peripheral sensory nerve endings.
Localization (release) of substance P in sensory nerve associated with substance p and morphine
7) Confidence 0.58 Published 1983 Journal Acta Physiol. Scand. Section Title Doc Link 6192685 Disease Relevance 0 Pain Relevance 1.17
Other studies suggest that this pain-suppression system involving the activation of mesolimbic DA neurons is naturally triggered by exposure to stress, through the endogenous release of opioids and substance P (SP) in the midbrain.
Localization (release) of substance P in midbrain associated with stress, pain, dopamine, midbrain, opioid and substance p
8) Confidence 0.58 Published 1999 Journal Life Sci. Section Abstract Doc Link 10597883 Disease Relevance 0.71 Pain Relevance 1.32
The uncadecapeptide substance P (SP), which is localized in peripheral and central terminals of afferent nerve fibers with polymodal nociceptors, has recently been implicated as having a neurogenic, inflammatory role in experimental arthritis.
Localization (localized) of substance P in nerve associated with inflammation, nociceptor, experimental arthritis, arthritis and substance p
9) Confidence 0.58 Published 1990 Journal Arthritis Rheum. Section Abstract Doc Link 1689161 Disease Relevance 0.96 Pain Relevance 0.71
In the spinal cord denervation supersensitivity to 5-HT may depend on reduced release of substance P (SP).
Localization (release) of substance P in spinal cord associated with substance p and spinal cord
10) Confidence 0.58 Published 1993 Journal Cephalalgia Section Abstract Doc Link 7684323 Disease Relevance 0.32 Pain Relevance 0.33
Capsaicin induces the release of substance P (SP) by PAFs, producing vasodilation and increasing vascular permeability (neurogenic inflammation).
Localization (release) of substance P associated with inflammation, qutenza, primary afferent fibers, neurogenic inflammation, increased venous pressure under development and substance p
11) Confidence 0.58 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.
Localization (releases) of substance-P associated with antagonist
12) Confidence 0.56 Published 2005 Journal Neurosci. Res. Section Abstract Doc Link 15927721 Disease Relevance 0.15 Pain Relevance 0.23
The facilitatory effect is indirect and involves tachykinin release and excitation of NK1 and NK3 receptors on cholinergic neurons.
Localization (release) of NK1 in cholinergic neurons
13) Confidence 0.50 Published 2006 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 16328494 Disease Relevance 0 Pain Relevance 0.64
Capsaicin in the adult animal is believed to evoke a massive release of substance P (SP) and a subsequent loss of primary afferent C-fiber activity.
Localization (release) of substance P associated with c fibre, qutenza and substance p
14) Confidence 0.49 Published 1994 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7509392 Disease Relevance 0.08 Pain Relevance 0.88
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.
Localization (release) of NK1 associated with qutenza and primary afferent fibers
15) Confidence 0.47 Published 2006 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 16328494 Disease Relevance 0 Pain Relevance 0.76
Capsaicin depolarizes primary afferent C-fibers releasing substance P (SP) whose N-terminal metabolites appear to play a role in the development of antinociception.
Localization (releasing) of substance P associated with antinociception, c fibre, qutenza and substance p
16) Confidence 0.46 Published 1999 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9918586 Disease Relevance 0 Pain Relevance 0.79
Inhibition of substance P release from spinal cord tissue after pretreatment with capsaicin does not mediate the antinociceptive effect of capsaicin in adult mice.
Localization (release) of substance P in spinal cord associated with qutenza, antinociceptive, spinal cord and substance p
17) Confidence 0.46 Published 1997 Journal Pain Section Title Doc Link 9231870 Disease Relevance 0.24 Pain Relevance 2.25
Substance P (SP) is released from primary afferent fibers in response to nociceptive stimuli.
Localization (released) of Substance P associated with nociception, primary afferent fibers and substance p
18) Confidence 0.46 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.19 Pain Relevance 1.18
Upon noxious stimulation, particularly intense stimulation, tachykinins such as SP and neurokinin A (NKA) are released from primary afferent fibers and excite dorsal horn neurons via activation of the neurokinin-1 and neurokinin-2 receptors (NK1R and NK2R), respectively [1,2].
Localization (released) of neurokinin in dorsal horn associated with primary afferent fibers, dorsal horn neuron and substance p
19) Confidence 0.44 Published 2005 Journal Mol Pain Section Body Doc Link PMC1315348 Disease Relevance 0.31 Pain Relevance 0.87
One is the exact location of NK1Rs on the neuron, since some studies report that NK1Rs are postsynaptically or extrasynaptically located [22].
Localization (location) of NK1Rs in neuron
20) Confidence 0.44 Published 2005 Journal Mol Pain Section Body Doc Link PMC1315348 Disease Relevance 0.23 Pain Relevance 0.69

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