INT13854

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Context Info
Confidence 0.50
First Reported 1982
Last Reported 2010
Negated 1
Speculated 2
Reported most in Abstract
Documents 13
Total Number 15
Disease Relevance 1.78
Pain Relevance 6.03

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
striatum 4
NAC 2
medulla 2
parasympathetic 2
hippocampus 2
Acot1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Potency 1 100.00 Very High Very High Very High
Nucleus accumbens 9 99.92 Very High Very High Very High
Pain 15 99.82 Very High Very High Very High
tetrodotoxin 17 99.74 Very High Very High Very High
Hippocampus 20 99.68 Very High Very High Very High
medulla 5 99.68 Very High Very High Very High
Dopamine 11 99.50 Very High Very High Very High
Inflammation 103 99.36 Very High Very High Very High
excitatory amino acid 6 98.88 Very High Very High Very High
Neurotransmitter 10 98.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pain 11 99.82 Very High Very High Very High
INFLAMMATION 102 99.36 Very High Very High Very High
Catalepsy 3 92.28 High High
Inflammatory Bowel Disease 1 91.56 High High
Nociception 1 90.84 High High
Clostridium Infection 1 85.88 High High
Paralysis 1 83.84 Quite High
Rheumatoid Arthritis 12 73.84 Quite High
Overactive Bladder 2 72.44 Quite High
Neurological Disease 1 63.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
TTX injected in the caudal ventrolateral medulla (CVLM) inhibited the phenylephrine-induced increase of ACh release.
Positive_regulation (phenylephrine-induced) of Positive_regulation (increase) of ACh in medulla associated with medulla and tetrodotoxin
1) Confidence 0.50 Published 1998 Journal Clin. Exp. Hypertens. Section Abstract Doc Link 9533616 Disease Relevance 0.08 Pain Relevance 0.94
Ovariectomy caused the significant increase in both TTX-insensitive basal Ach release and TTX-insensitive stretch-induced Ach release.
Positive_regulation (increase) of Positive_regulation (stretch-induced) of Ach
2) Confidence 0.50 Published 2007 Journal Neurourol. Urodyn. Section Body Doc Link 17480029 Disease Relevance 0.14 Pain Relevance 0
When perfused in the MS/VDB, the excitatory amino-acid agonists N-methyl-D-aspartate (NMDA) (100 mumol/l) and kainic acid (10 mumol/l) caused an increase in the extracellular level of ACh in the hippocampus by 83% and 161%, respectively.
Positive_regulation (caused) of Positive_regulation (increase) of ACh in hippocampus associated with agonist and hippocampus
3) Confidence 0.46 Published 1994 Journal Brain Res. Section Abstract Doc Link 7922524 Disease Relevance 0 Pain Relevance 0.66
These data suggest that haloperidol-induced release of DA is, at least partially, mediated by the activation of muscarinic ACh receptors located in the striatum.
Spec (partially) Positive_regulation (mediated) of Positive_regulation (activation) of ACh in striatum associated with dopamine
4) Confidence 0.44 Published 1990 Journal Neuropharmacology Section Abstract Doc Link 2304616 Disease Relevance 0 Pain Relevance 0.54
In both sexes the Novelty and Object tests induced an increase in ACh levels with respect to Baseline.
Positive_regulation (induced) of Positive_regulation (increase) of ACh
5) Confidence 0.41 Published 1999 Journal Brain Res. Section Abstract Doc Link 9878722 Disease Relevance 0.21 Pain Relevance 0.28
In females, the pain-induced increase of ACh was delayed and increased by exposure to lemon essential oil.
Positive_regulation (increased) of Positive_regulation (increase) of ACh associated with pain
6) Confidence 0.41 Published 2002 Journal Neurosci. Lett. Section Abstract Doc Link 12213626 Disease Relevance 0.29 Pain Relevance 0.36
Low concentrations of THA (300 nM-3 microM) caused a small inward current and a 10-fold increase in the potency of ACh to produce inward (excitatory) currents.
Positive_regulation (caused) of Positive_regulation (increase) of ACh associated with potency
7) Confidence 0.25 Published 1996 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 8558423 Disease Relevance 0 Pain Relevance 0.44
Tetrodotoxin blocked the increase in the release and synthesis of ACh induced by tityustoxin.
Positive_regulation (increase) of Positive_regulation (induced) of ACh associated with tetrodotoxin
8) Confidence 0.24 Published 1982 Journal Toxicon Section Abstract Doc Link 6808708 Disease Relevance 0 Pain Relevance 0.28
The QUIS (100 microM) perfused through the striatum induced an increase of extracellular ACh level (250%) which lasted for over 1h and gradually returned to basal values.
Positive_regulation (induced) of Positive_regulation (increase) of ACh in striatum
9) Confidence 0.24 Published 2002 Journal Neurochem. Int. Section Abstract Doc Link 11821149 Disease Relevance 0 Pain Relevance 0.23
L-Glu did not inhibit the activity of acetylcholinesterase, therefore the postjunctional potentiation was not due to ACh accumulation.
Neg (not) Positive_regulation (due) of Positive_regulation (accumulation) of ACh
10) Confidence 0.19 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2568940 Disease Relevance 0 Pain Relevance 0.29
Thus, accumulation of ACh is likely to be caused by non-quantal release from cholinergic terminals.
Spec (likely) Positive_regulation (caused) of Positive_regulation (accumulation) of ACh
11) Confidence 0.12 Published 2010 Journal Exp. Physiol. Section Abstract Doc Link 19767403 Disease Relevance 0.09 Pain Relevance 0.17
The present data reveal that neuronal activity in the NAC is necessary for behaviorally induced increases in cortical ACh efflux and that this activation does not require increases in D2 receptor activity.
Positive_regulation (necessary) of Positive_regulation (increases) of ACh in NAC associated with nucleus accumbens
12) Confidence 0.10 Published 2004 Journal Neuroscience Section Abstract Doc Link 14706776 Disease Relevance 0 Pain Relevance 0.59
The release of [3H]ACh induced by concentrations of PTX less than 10(-10) M was more dependent on the simultaneous presence of both Ca2+ and Na+ than the release induced by higher concentrations of PTX.
Positive_regulation (dependent) of Positive_regulation (induced) of ACh
13) Confidence 0.08 Published 1991 Journal J. Neurochem. Section Abstract Doc Link 1680161 Disease Relevance 0 Pain Relevance 0.14
Inhibition of Na/K ATPase by ouabain led to an increase of striatal acetylcholine (Ach) release, which was enhanced by Met-enkephalin.
Positive_regulation (led) of Positive_regulation (increase) of Ach associated with enkephalin
14) Confidence 0.06 Published 1985 Journal Pol J Pharmacol Pharm Section Abstract Doc Link 2999739 Disease Relevance 0.26 Pain Relevance 0.61
Similar to the experimental setting, this decrease could be caused by central activation of the vagus and peripheral increase in ACh, the main anti-inflammatory neurotransmitter released by parasympathetic fibers.
Positive_regulation (activation) of Positive_regulation (increase) of ACh in parasympathetic associated with neurotransmitter and inflammation
15) Confidence 0.01 Published 2010 Journal Curr Rheumatol Rep Section Body Doc Link PMC2927688 Disease Relevance 0.71 Pain Relevance 0.50

General Comments

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