INT45433

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.45
First Reported 1984
Last Reported 2010
Negated 3
Speculated 0
Reported most in Abstract
Documents 18
Total Number 18
Disease Relevance 1.90
Pain Relevance 4.32

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) mitochondrion (Acot1) lipid metabolic process (Acot1)
cytoplasm (Acot1)
Anatomy Link Frequency
reticular formation 6
neuronal 2
ASM 2
neurons 2
brain 2
Acot1 (Mus musculus)
Pain Link Frequency Relevance Heat
Serotonin 78 99.98 Very High Very High Very High
Potency 2 99.90 Very High Very High Very High
calcitonin gene related peptide 24 99.80 Very High Very High Very High
antagonist 37 99.74 Very High Very High Very High
isoflurane 10 99.70 Very High Very High Very High
Neurotransmitter 20 98.08 Very High Very High Very High
anesthesia 13 97.88 Very High Very High Very High
tetrodotoxin 10 93.12 High High
agonist 33 93.04 High High
halothane 7 87.12 High High
Disease Link Frequency Relevance Heat
Asthma 74 94.84 High High
Disease 125 88.04 High High
INFLAMMATION 63 83.44 Quite High
Ganglion Cysts 4 78.20 Quite High
Bronchitis 9 76.36 Quite High
Occupational Lung Diseases 18 73.12 Quite High
Poisoning 3 72.84 Quite High
Rhinitis 7 62.64 Quite High
Heart Rate Under Development 5 61.76 Quite High
Bronchospasm 2 52.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Nitric oxide (NO)-releasing beads microinjected into the pontine reticular formation of C57BL/6J (B6) mice significantly (P < 0.0001) increased ACh release.
Positive_regulation (increased) of Localization (release) of ACh in reticular formation
1) Confidence 0.45 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0
Together, these neurochemical and EEG data support the conclusion that M2 autoreceptor enhancement of ACh release in prefrontal cortex activates EEG in contralateral prefrontal cortex of B6 mouse.
Positive_regulation (enhancement) of Localization (release) of ACh in cortex
2) Confidence 0.43 Published 2002 Journal J. Neurophysiol. Section Abstract Doc Link 12037184 Disease Relevance 0 Pain Relevance 0.17
Dialysis delivery of relatively subtype selective muscarinic antagonists to the PnO revealed the following order of potency for increasing ACh release: scopolamine (3 nM)>AF-DX 116 (100 nM)=pirenzepine (100 nM).
Positive_regulation (increasing) of Localization (release) of ACh associated with antagonist and potency
3) Confidence 0.40 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.34
The muscarinic antagonist scopolamine increased ACh release in the PnO by 21% (3 nM), 48% (10 nM), 56% (30 nM), and 104% (100 nM).
Positive_regulation (increased) of Localization (release) of ACh associated with antagonist
4) Confidence 0.40 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.36
Microdialysis delivery of the NO donor N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino)-ethanamine (NOC-12) to the mouse pontine reticular formation also caused a concentration-dependent increase in ACh release (P < 0.001).
Positive_regulation (increase) of Localization (release) of ACh in reticular formation
5) Confidence 0.39 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.05
Microdialysis delivery of the NO donor N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino)-ethanamine (NOC-12) to the mouse pontine reticular formation also caused a concentration-dependent increase in ACh release (P < 0.001).
Positive_regulation (caused) of Localization (release) of ACh in reticular formation
6) Confidence 0.39 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.05
Under the latter conditions of pretreatment, veratridine then stimulated the Ca2+-independent release of ACh even more, but did not stimulate the release of choline.
Neg (not) Positive_regulation (stimulated) of Localization (release) of ACh
7) Confidence 0.39 Published 1984 Journal Brain Res. Section Abstract Doc Link 6697191 Disease Relevance 0 Pain Relevance 0.07
These results suggest that depolarization of brain tissue does not facilitate the Ca2+-independent release of ACh from the cytoplasm because a portion of ACh stored there is hydrolyzed.
Neg (not) Positive_regulation (facilitate) of Localization (release) of ACh in brain
8) Confidence 0.39 Published 1984 Journal Brain Res. Section Abstract Doc Link 6697191 Disease Relevance 0 Pain Relevance 0.07
Following this expansion of the S3 ACh content, veratridine caused an even greater loss of S3 ACh, and increased the Ca2+-independent release of ACh slightly.
Positive_regulation (increased) of Localization (release) of ACh
9) Confidence 0.39 Published 1984 Journal Brain Res. Section Abstract Doc Link 6697191 Disease Relevance 0 Pain Relevance 0.09
High levels of extracellular ACh are accompanied by reduced levels of extracellular choline, and ACh release becomes strongly dependent on choline availability.
Positive_regulation (dependent) of Localization (release) of ACh
10) Confidence 0.27 Published 2008 Journal Neurochem. Int. Section Abstract Doc Link 18023504 Disease Relevance 0 Pain Relevance 0.12
Dialysis delivery of bicuculline to the PnO of male mice (n = 18) anesthetized with isoflurane significantly increased ACh release in the PnO, decreased breathing rate, and increased anesthesia recovery time.
Positive_regulation (increased) of Localization (release) of ACh associated with anesthesia and isoflurane
11) Confidence 0.14 Published 2010 Journal J. Neurosci. Section Abstract Doc Link 20844126 Disease Relevance 0 Pain Relevance 0.56
Stimulation of 5HT4 receptors by serotonin augments the release of Ach and CGRP.
Positive_regulation (augments) of Localization (release) of Ach associated with calcitonin gene related peptide and serotonin
12) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503665 Disease Relevance 0.08 Pain Relevance 0.70
Stimulation of 5HT4 receptors on submucosal IPANs by serotonin augments the release of Ach and CGRP.
Positive_regulation (augments) of Localization (release) of Ach associated with calcitonin gene related peptide and serotonin
13) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503665 Disease Relevance 0.07 Pain Relevance 0.66
Presynaptic 5HT4 receptors also augment this Ach release (Grider 1996; Gershon 2004, 2005).
Positive_regulation (augment) of Localization (release) of Ach
14) Confidence 0.09 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503665 Disease Relevance 0.06 Pain Relevance 0.57
Our electrophysiological approach, while not measuring ACh release directly, does indicate ‘effective’ release, i.e. that which leads to membrane depolarization.
Neg (not) Positive_regulation (measuring) of Localization (release) of ACh
15) Confidence 0.08 Published 2008 Journal The Journal of Physiology Section Body Doc Link PMC2538785 Disease Relevance 0.07 Pain Relevance 0.11
This secretion mediated by PAR(1) probably occurred by activation of the receptor on the submucosal secretomotor neurons, resulting mainly in the release of tachykinins and activation of the neurokinin-1 receptor, and partly in the release of ACh and activation of the muscarinic and nicotinic receptors.
Positive_regulation (resulting) of Localization (release) of ACh in neurons
16) Confidence 0.05 Published 2010 Journal Am. J. Physiol. Gastrointest. Liver Physiol. Section Abstract Doc Link 20413722 Disease Relevance 0 Pain Relevance 0.31
Following the release of acetylcholine (Ach) from cholinergic nerve endings, Ach binds to M3 receptors on ASM cells; further release of Ach is halted through the activity of M2 receptors on cholinergic nerve endings, limiting ASM constriction [16].
Positive_regulation (Following) of Localization (release) of Ach in ASM
17) Confidence 0.03 Published 2008 Journal Allergy Asthma Clin Immunol Section Body Doc Link PMC2868889 Disease Relevance 1.55 Pain Relevance 0.08
In contrast, treatment with BDNF activates neuronal p75NTR, inducing the release of ACh and significantly slowing the rate of myocyte contraction [194].
Positive_regulation (inducing) of Localization (release) of ACh in neuronal
18) Confidence 0.01 Published 2010 Journal The Open Biochemistry Journal Section Body Doc Link PMC2864432 Disease Relevance 0.06 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox