INT20721

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Context Info
Confidence 0.80
First Reported 1989
Last Reported 2010
Negated 1
Speculated 0
Reported most in Abstract
Documents 47
Total Number 47
Disease Relevance 11.37
Pain Relevance 10.95

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

cytosol (ACOT1) lipid metabolic process (ACOT1) cytoplasm (ACOT1)
Anatomy Link Frequency
neuronal 7
nerve 6
bladder 2
cholinergic neurons 2
spinal cord 1
ACOT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Neurotransmitter 54 100.00 Very High Very High Very High
Morphine 4 99.92 Very High Very High Very High
Spinal cord 5 99.84 Very High Very High Very High
analgesia 14 99.72 Very High Very High Very High
tetrodotoxin 20 99.48 Very High Very High Very High
Endogenous opioid 1 99.46 Very High Very High Very High
Opioid 7 99.40 Very High Very High Very High
Dorsal horn 1 99.36 Very High Very High Very High
Clonidine 1 98.88 Very High Very High Very High
conotoxin 18 98.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypersensitivity 210 99.80 Very High Very High Very High
Paralysis 96 99.44 Very High Very High Very High
Diabetes Mellitus 137 98.68 Very High Very High Very High
Stress 30 98.04 Very High Very High Very High
Helminth Infection 154 97.38 Very High Very High Very High
Pain 311 96.64 Very High Very High Very High
Asthma 26 95.52 Very High Very High Very High
Occupational Lung Diseases 17 93.64 High High
Targeted Disruption 111 92.76 High High
Cognitive Disorder 57 92.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The finding that high concentrations of synthetic opioids or opioid antagonists were required to inhibit output suggests that they may not be acting specifically, and provides no evidence for the hypothesis that endogenous opioids play a role in control of ACh release into fetal vessels of human placentae.
Localization (release) of ACh in vessels associated with antagonist, endogenous opioid and opioid
1) Confidence 0.80 Published 1989 Journal Placenta Section Abstract Doc Link 2674931 Disease Relevance 0 Pain Relevance 1.01
The data demonstrate that LA-N-2 cells exhibit some properties similar to cholinergic neurons and may therefore be useful for studies of ACh synthesis and release.
Localization (release) of ACh in cholinergic neurons
2) Confidence 0.61 Published 1989 Journal Brain Res. Section Abstract Doc Link 2702472 Disease Relevance 0.07 Pain Relevance 0.09
The cells release ACh spontaneously and this release is enhanced upon depolarization with potassium or veratridine (the latter effect is blocked by tetrodotoxin).
Localization (release) of ACh associated with tetrodotoxin
3) Confidence 0.61 Published 1989 Journal Brain Res. Section Abstract Doc Link 2702472 Disease Relevance 0.07 Pain Relevance 0.09
We have investigated the rates of acetylcholine (ACh) synthesis and release in LA-N-2 cells in order to characterize them as a potential model of cholinergic neurons.
Localization (release) of ACh in cholinergic neurons
4) Confidence 0.61 Published 1989 Journal Brain Res. Section Abstract Doc Link 2702472 Disease Relevance 0.07 Pain Relevance 0
The cells release ACh spontaneously and this release is enhanced upon depolarization with potassium or veratridine (the latter effect is blocked by tetrodotoxin).
Localization (release) of ACh associated with tetrodotoxin
5) Confidence 0.61 Published 1989 Journal Brain Res. Section Abstract Doc Link 2702472 Disease Relevance 0.07 Pain Relevance 0.10
The two inhibitors of ACh release, morphine (0.3 microM) and clonidine (0.4 microM), antagonized EC(50) AFB(1)-induced contractions, and apamin, a drug that increases neuronal excitability, facilitated the EC(50) AFB(1)-induced contractile effect.
Localization (release) of ACh in neuronal associated with neuronal excitability, clonidine and morphine
6) Confidence 0.57 Published 2002 Journal Toxicol In Vitro Section Abstract Doc Link 12206819 Disease Relevance 0 Pain Relevance 0.34
Electrical field stimulation (EFS) of human airways, in vitro, evokes cholinergic contraction mediated by the release of acetylcholine (Ach) from postganglionic cholinergic nerves.
Localization (release) of Ach in nerves
7) Confidence 0.57 Published 1999 Journal Eur. Respir. J. Section Abstract Doc Link 10543288 Disease Relevance 0.35 Pain Relevance 0.09
In addition, the modulation of NE release by adrenoceptor ligands displayed the appropriate pharmacology of alpha-2 autoreceptors; ACh release was modulated by muscarinic ligands.
Localization (release) of ACh
8) Confidence 0.55 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0.08 Pain Relevance 0.32
The peptide modulator of the N-type voltage sensitive Ca++ channel, omega-conotoxin GVIA, inhibited NE release with an IC50 of about 14 nM and ACh release with an IC50 of about 3 nM, whereas L-type modulators were ineffective.
Localization (release) of ACh associated with conotoxin
9) Confidence 0.48 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0.06 Pain Relevance 0.31
Thus, the action potential-induced, exocytotic tritium overflow supports the assumption of a quasiphysiological release of NE from noradrenergic and of acetylcholine (ACh) from cholinergic nerve terminals, respectively.
Localization (release) of ACh in nerve associated with action potential
10) Confidence 0.48 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0.09 Pain Relevance 0.33
The effects of drugs on NE and ACh release were not age-related.
Localization (release) of ACh
11) Confidence 0.48 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0.07 Pain Relevance 0.32
Both NE and ACh release decreased with the age of the patients.
Localization (release) of ACh
12) Confidence 0.48 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0.07 Pain Relevance 0.32
In conclusion, Ca++ entry through N-type Ca++ channels, rather then L-type Ca++ channels, predominates in subserving NE and ACh release from noradrenergic and cholinergic nerve terminals, respectively, of human neocortex.
Localization (release) of ACh in nerve
13) Confidence 0.48 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0 Pain Relevance 0.14
Furthermore, any flow-induced release of endogenous ACh from the endothelial cells may, at least in part, contribute to the sustained elevation of plasma NO concentration.
Localization (release) of ACh in endothelial cells
14) Confidence 0.45 Published 2010 Journal European Heart Journal Section Body Doc Link PMC2995954 Disease Relevance 0.39 Pain Relevance 0.04
Intravenous opioids cause analgesia and increase release of ACh in spinal cord dorsal horn in animals, and these effects are enhanced by intrathecal neostigmine injection.
Localization (release) of ACh in spinal cord dorsal horn associated with dorsal horn, opioid, intrathecal, spinal cord and analgesia
15) Confidence 0.30 Published 1997 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9223543 Disease Relevance 0 Pain Relevance 0.76
There was tetrodotoxin-insensitive non-neuronal ACh release and this was significantly higher in strips with urothelium than in strips without urothelium.
Localization (release) of ACh in neuronal associated with tetrodotoxin
16) Confidence 0.29 Published 2008 Journal J. Pharmacol. Sci. Section Abstract Doc Link 18285653 Disease Relevance 0 Pain Relevance 0.10
The stretch-induced release of non-neuronal ACh was increased with age.
Localization (release) of ACh in neuronal
17) Confidence 0.29 Published 2008 Journal J. Pharmacol. Sci. Section Abstract Doc Link 18285653 Disease Relevance 0 Pain Relevance 0.09
The non-neuronal ACh release was increased with age.
Localization (release) of ACh in neuronal
18) Confidence 0.29 Published 2008 Journal J. Pharmacol. Sci. Section Abstract Doc Link 18285653 Disease Relevance 0 Pain Relevance 0.09
Stretch of bladder strips caused increases in non-neuronal ACh release.
Localization (release) of ACh in bladder
19) Confidence 0.29 Published 2008 Journal J. Pharmacol. Sci. Section Abstract Doc Link 18285653 Disease Relevance 0 Pain Relevance 0.09
Recently, several reports demonstrate that non-neuronal acetylcholine (ACh) release may contribute to various pathophysiological conditions.
Localization (release) of ACh in neuronal
20) Confidence 0.29 Published 2008 Journal J. Pharmacol. Sci. Section Abstract Doc Link 18285653 Disease Relevance 0 Pain Relevance 0

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