INT8534

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Context Info
Confidence 0.59
First Reported 1990
Last Reported 2010
Negated 1
Speculated 1
Reported most in Abstract
Documents 85
Total Number 87
Disease Relevance 28.71
Pain Relevance 82.82

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

cell proliferation (Pax3) nucleus (Pax3) DNA binding (Pax3)
Anatomy Link Frequency
neurons 4
nerves 4
lens 3
sensory nerves 3
spinal cord 3
Pax3 (Mus musculus)
Pain Link Frequency Relevance Heat
substance P 2309 100.00 Very High Very High Very High
Neuropeptide 347 100.00 Very High Very High Very High
Glutamate 271 100.00 Very High Very High Very High
Calcitonin gene-related peptide 162 100.00 Very High Very High Very High
calcitonin gene related peptide 137 100.00 Very High Very High Very High
bradykinin 73 100.00 Very High Very High Very High
c fibre 143 99.98 Very High Very High Very High
primary afferent fibers 144 99.92 Very High Very High Very High
qutenza 1192 99.84 Very High Very High Very High
Pain 607 99.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pain 640 99.84 Very High Very High Very High
Nociception 461 99.82 Very High Very High Very High
INFLAMMATION 587 99.40 Very High Very High Very High
Cystitis 60 99.28 Very High Very High Very High
Disease 95 99.20 Very High Very High Very High
Neurogenic Inflammation 36 98.98 Very High Very High Very High
Hypersensitivity 38 98.88 Very High Very High Very High
Hyperalgesia 143 98.74 Very High Very High Very High
Increased Venous Pressure Under Development 74 98.52 Very High Very High Very High
Colitis 84 97.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These data indicate that antinociception does not appear to depend on decreases in SP release or content as antinociception precedes decreases in SP release.
Localization (release) of SP associated with antinociception and substance p
1) Confidence 0.59 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.07 Pain Relevance 2.16
In contrast, capsaicin-evoked SP release decreased significantly in tissue from mice pretreated with capsaicin or SP(1-7) 48 h prior to testing.
Localization (release) of SP associated with qutenza and substance p
2) Confidence 0.59 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.21 Pain Relevance 2.83
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 SP associated with antinociception, c fibre, qutenza and substance p
3) Confidence 0.57 Published 1999 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9918586 Disease Relevance 0 Pain Relevance 0.79
These results suggest a possible mechanism by which pain-evoked release of SP may sustain opioid analgesia by attenuating the development of tolerance and inhibiting the expression of withdrawal.
Localization (release) of SP associated with pain, tolerance, withdrawal, opioid, analgesia and substance p
4) Confidence 0.54 Published 1996 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 8930169 Disease Relevance 0.15 Pain Relevance 2.03
Capsaicin pretreatment decreases the content and release of SP from primary afferent fibers.
Localization (release) of SP associated with qutenza, primary afferent fibers and substance p
5) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.24 Pain Relevance 1.76
Capsaicin, which produces an initial hyperalgesic response followed by persistent antinociception, also elicits release of SP from primary afferent fibers.
Localization (release) of SP associated with antinociception, hyperalgesia, qutenza, primary afferent fibers and substance p
6) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.19 Pain Relevance 1.63
D-Substance P(1-7), which prevents antinociception, blocked capsaicin- and SP(1-7)-induced decreases in SP release, indicating that these effects are mediated by SP N-terminal activity.
Localization (release) of SP associated with antinociception, qutenza and substance p
7) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.13 Pain Relevance 2.68
Substance P (SP) is released from primary afferent fibers in response to nociceptive stimuli.
Localization (released) of SP associated with nociception, primary afferent fibers and substance p
8) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.19 Pain Relevance 1.18
These data indicate that antinociception does not appear to depend on decreases in SP release or content as antinociception precedes decreases in SP release.
Localization (release) of SP associated with antinociception and substance p
9) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.07 Pain Relevance 2.27
N-terminal metabolic fragments of SP that accumulate after capsaicin-induced SP release and are involved in the antinociceptive effect of capsaicin, were also tested.
Localization (release) of SP associated with qutenza, antinociceptive and substance p
10) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.24 Pain Relevance 2.52
However, at this time there was no decrease in capsaicin-evoked release of SP in tissue from capsaicin- and SP(1-7)-pretreated animals compared to those injected with vehicle.
Localization (release) of SP associated with qutenza and substance p
11) Confidence 0.52 Published 1997 Journal Pain Section Abstract Doc Link 9231870 Disease Relevance 0.23 Pain Relevance 2.80
Importantly, based on the intensities of stimuli required to evoke internalization, we conclude that SP is only released under conditions in which severe pain would be produced, that the release can be evoked by intense stimulation of somatic and visceral tissue, and that multiple stimulus modalities are effective.
Localization (released) of SP in visceral associated with pain and substance p
12) Confidence 0.51 Published 1999 Journal Reg Anesth Pain Med Section Abstract Doc Link 9952097 Disease Relevance 0.77 Pain Relevance 0.86
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 SP associated with c fibre, qutenza and substance p
13) Confidence 0.49 Published 1994 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7509392 Disease Relevance 0.08 Pain Relevance 0.89
The antinociceptive effect of capsaicin in the adult animal is, therefore, mimicked by SP(1-7) and attenuated by [D-Pro2,D-Phe7]-SP(1-7), suggesting that the NH2-terminus of SP and its NH2-terminal metabolites, released in response to capsaicin, may contribute to the mediation of capsaicin's antinociceptive effect.
Localization (released) of SP associated with qutenza, antinociceptive and substance p
14) Confidence 0.49 Published 1994 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7509392 Disease Relevance 0.06 Pain Relevance 1.82
Substance P (SP) is released in response to noxious stimuli.
Localization (released) of SP associated with substance p
15) Confidence 0.49 Published 1996 Journal Pain Section Abstract Doc Link 8951939 Disease Relevance 0.41 Pain Relevance 0.59
In the present study, the nociception induced by SP (and N/OFQ) was abolished by intrathecal (i.t.) injection of neurokinin(1) (SP receptor) antagonist, suggesting the involvement of the stimulation of nociceptive primary SP neuron and SP release into spinal synapses.
Localization (release) of SP in SP neuron associated with nociception, antagonist, intrathecal and substance p
16) Confidence 0.48 Published 1999 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 10490918 Disease Relevance 0.59 Pain Relevance 0.97
In the present study, the nociception induced by SP (and N/OFQ) was abolished by intrathecal (i.t.) injection of neurokinin(1) (SP receptor) antagonist, suggesting the involvement of the stimulation of nociceptive primary SP neuron and SP release into spinal synapses.
Localization (release) of SP in SP neuron associated with nociception, antagonist, intrathecal and substance p
17) Confidence 0.48 Published 1999 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 10490918 Disease Relevance 0.59 Pain Relevance 0.97
By following internalization of the SP receptor in spinal cord dorsal horn neurons, we have identified the stimuli that evoke SP release and the neurons that respond to these stimuli.
Localization (release) of SP in neurons associated with dorsal horn neuron, spinal cord and substance p
18) Confidence 0.44 Published 1999 Journal Reg Anesth Pain Med Section Abstract Doc Link 9952097 Disease Relevance 0.70 Pain Relevance 0.81
We previously reported that the intraplantar (i.pl.) application of nociceptin/orphanin FQ (N/OFQ) at extremely low doses elicited a nociception through a substance P (SP) release from nociceptor endings.
Localization (release) of SP in nociceptor associated with nociception, nociceptor, orphanin and substance p
19) Confidence 0.42 Published 1999 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 10490918 Disease Relevance 0.48 Pain Relevance 0.87
If an antinociceptive role for SP-driven feed-forward inhibition exists, the activation of SP release would have an analgesic effect in SP-SAP injected animals but blocking SP transmission would result in behavioral sensitization in SP-SAP injected animals.
Localization (release) of SP associated with analgesic, antinociceptive and substance p
20) Confidence 0.26 Published 2005 Journal Mol Pain Section Body Doc Link PMC1315348 Disease Relevance 0.38 Pain Relevance 1.49

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