INT4735

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Context Info
Confidence 0.71
First Reported 1980
Last Reported 2010
Negated 1
Speculated 0
Reported most in Abstract
Documents 80
Total Number 80
Disease Relevance 13.22
Pain Relevance 26.68

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
hippocampus 8
neurons 6
cortex 5
striatum 4
neuronal 4
Acot1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Neurotransmitter 76 100.00 Very High Very High Very High
gABA 72 100.00 Very High Very High Very High
Glutamate 55 100.00 Very High Very High Very High
tetrodotoxin 39 100.00 Very High Very High Very High
Enkephalin 25 100.00 Very High Very High Very High
substance P 18 100.00 Very High Very High Very High
Pain 17 99.96 Very High Very High Very High
dopamine receptor 1 99.96 Very High Very High Very High
cerebral cortex 74 99.84 Very High Very High Very High
opioid receptor 9 99.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 161 100.00 Very High Very High Very High
Urological Neuroanatomy 80 99.96 Very High Very High Very High
Pain 23 99.96 Very High Very High Very High
Cognitive Disorder 101 99.76 Very High Very High Very High
Hepatic Encephalopathy 136 99.66 Very High Very High Very High
Depression 4 99.62 Very High Very High Very High
Frailty 131 99.08 Very High Very High Very High
Liver Failure 80 98.86 Very High Very High Very High
Paralysis 4 98.56 Very High Very High Very High
Hypertension 11 98.50 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A study was made of the effects of several monoamine-uptake inhibitors on membrane currents elicited by acetylcholine (ACh-currents) generated by rat neuronal alpha2beta4 and mouse muscle nicotinic acetylcholine receptors (AChRs) expressed in Xenopus laevis oocytes.
Gene_expression (expressed) of AChRs in neuronal associated with monoamine
1) Confidence 0.71 Published 2001 Journal Mol. Psychiatry Section Abstract Doc Link 11526465 Disease Relevance 0 Pain Relevance 0.36
Changes in hippocampal Ach and Ch levels were observed in both cognition markedly impaired group and cognition lightly impaired group, accompanied by performance failure in water maze test.
Gene_expression (levels) of Ach
2) Confidence 0.67 Published 2009 Journal Zhonghua Yi Xue Za Zhi Section Body Doc Link 20095350 Disease Relevance 0.07 Pain Relevance 0
The extracellular levels of ACh in the dorsal hippocampus were estimated by measurement of its concentration in the perfusion fluid by high-performance liquid chromatography with electrochemical detection.
Gene_expression (levels) of ACh in hippocampus associated with hippocampus
3) Confidence 0.60 Published 1997 Journal Brain Res. Section Abstract Doc Link 9067465 Disease Relevance 0.32 Pain Relevance 0.21
However, in the same preparation, increasing concentrations (from 1 to 1000 nmol) of ACh produced only the long-lasting vasodilator responses in a concentration-dependent manner.
Gene_expression (produced) of ACh
4) Confidence 0.59 Published 1995 Journal Circ. Res. Section Abstract Doc Link 7758164 Disease Relevance 0.36 Pain Relevance 0.49
Inhalational general anesthetics have recently been shown to inhibit neuronal nicotinic acetylcholine (ACh) receptors (nnAChRs) expressed in Xenopus laevis oocytes and in molluscan neurons.
Gene_expression (expressed) of ACh in neuronal
5) Confidence 0.53 Published 2001 Journal Mol. Pharmacol. Section Abstract Doc Link 11259617 Disease Relevance 0 Pain Relevance 0.10
These results support the suggestion that barbiturates primarily inhibit the Ca-dependent stimulated release of ACh and affect ACh synthesis only indirectly.
Gene_expression (synthesis) of ACh
6) Confidence 0.53 Published 1980 Journal Neurochem. Res. Section Abstract Doc Link 6968410 Disease Relevance 0 Pain Relevance 0.16
The effects of oxotremorine and the cyclic GMP derivatives were not due to diminished ACh synthesis, since these compounds did not influence the reduction of tissue ACh resulting from treatment with K+ and atropine.
Gene_expression (synthesis) of ACh
7) Confidence 0.53 Published 1980 Journal Brain Res. Section Abstract Doc Link 6243230 Disease Relevance 0 Pain Relevance 0.09
The results are discussed and related to the circadian rhythms that were demonstrated in brain levels of ACh, in opioid receptors and in the secretion of opioid peptides.
Gene_expression (levels) of ACh in brain associated with opioid receptor and opioid
8) Confidence 0.52 Published 1982 Journal Arch Int Pharmacodyn Ther Section Abstract Doc Link 7181581 Disease Relevance 0 Pain Relevance 0.46
Three experiments using rats as subjects were designed to test hypotheses about relationships among lithium, ACh synthesis and behavior.
Gene_expression (synthesis) of ACh
9) Confidence 0.52 Published 1981 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 6785802 Disease Relevance 0 Pain Relevance 0
Suppression of behavior accompanying increased ACh synthesis in the brain might account, at least in part, for the preferred use of lithium in antimanic therapy.
Gene_expression (synthesis) of ACh in brain
10) Confidence 0.52 Published 1981 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 6785802 Disease Relevance 0 Pain Relevance 0
Morphine elevated the levels of ACh in the cerebellum and striatum, cold water swimming--in the cerebellum, striatum and cortex, and physostigmine--in the striatum and hippocampus.
Gene_expression (levels) of ACh in striatum associated with hippocampus and morphine
11) Confidence 0.52 Published 1983 Journal Neuropharmacology Section Abstract Doc Link 6621812 Disease Relevance 0 Pain Relevance 1.00
Local perfusion of 1 mumol/l of the sodium-channel blocker tetrodotoxin (TTX) through the probe resulted in 94% and 92% decrease in extracellular levels of ACh in the hippocampus and the septal area, respectively.
Gene_expression (levels) of ACh in septal area associated with tetrodotoxin and hippocampus
12) Confidence 0.52 Published 1994 Journal Brain Res. Section Abstract Doc Link 7922524 Disease Relevance 0 Pain Relevance 0.50
Interruption of the corticostriatal pathway by undercutting the cortex resulted in a reduction of glutamate uptake by 55% and in a depression of acetylcholine (ACh) synthesis by 30% in striatum after two postlesion weeks without affecting the content of ACh and choline, the specific binding of [3H]dexetimide to muscarinic receptors, the activity of choline acetyltransferase and the levels of noradrenaline, serotonin, dopamine and 3,4-dihydroxyphenylacetic acid.
Gene_expression (synthesis) of ACh in cortex associated with dopamine, glutamate, depression, noradrenaline and serotonin
13) Confidence 0.51 Published 1986 Journal Brain Res. Section Abstract Doc Link 3004639 Disease Relevance 0.10 Pain Relevance 0.32
The 5HT1A agonist 8-OH-DPAT given systemically again decreased extracellular levels of ACh, and the effect was dose-dependent.
Gene_expression (levels) of ACh associated with agonist
14) Confidence 0.51 Published 1993 Journal Brain Res. Section Abstract Doc Link 8374797 Disease Relevance 0 Pain Relevance 0.53
Using an in vitro microsuperfusion procedure, the release of newly synthesized [(3)H]-acetylcholine (ACh), evoked by N-methyl-D-aspartate (NMDA) receptor stimulation, was investigated in striosome-enriched areas and matrix of the rat striatum.
Gene_expression (synthesized) of ACh in striatum
15) Confidence 0.50 Published 2004 Journal Neuroscience Section Abstract Doc Link 14706785 Disease Relevance 0 Pain Relevance 0.37
Acetylcholine (ACh) in gastric juice was detected and measured by pretreatment of acetylcholinesterase inhibitor, 1 mM eserine (1 ml/rat, p.o.), in pylorus-ligated rats, by liquid chromatography with electrochemical detection.
Gene_expression (detected) of ACh in gastric juice
16) Confidence 0.48 Published 2000 Journal J. Chromatogr. B Biomed. Sci. Appl. Section Abstract Doc Link 10901134 Disease Relevance 0 Pain Relevance 0
The results showed: (1) Pain stimulation increased norepinephrine (NE), but not epinephrine, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DA metabolic product), homovanilic acid (DA metabolic product), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HT metabolic product), acetycholine (Ach), choline (Ach metabolic product), gamma-aminobutyric acid (GABA), and L-glutamate acid concentrations in the PVN perfusion liquid; (2) PVN stimulation with L-glutamate sodium, which excited local neurons only, did not influence the concentrations of the studied classical neurotransmitter and metabolic product in the PVN perfusion liquid; (3) Microinjection of NE, epinephrine, or L-glutamate sodium into the PVN elevated pain threshold, and local administration of GABA decreased pain threshold in a dose-dependent manner, but PVN administration of Ach, DA, or 5-HT did not change pain threshold; (4) Microinjection of phentolamine (alpha-receptor antagonist) or MK801 [NMDA-receptor antagonist] into the PVN reduced pain threshold, and local administration of bicuculline (GABA-receptor antagonist) raised pain threshold, but PVN administration of propranolol (beta-receptor antagonist), atropine (Muscarinic cholinergic receptor antagonist), 6-OH gallamine (Nicotinic cholinergic receptor antagonist), fluperidol (DA-receptor antagonist), or cyproheptadine (5-HT-receptor antagonist) did not alter pain threshold.
Gene_expression (product) of Ach in neurons associated with pain, pain threshold, neurotransmitter, glutamate, gaba, dopamine, antagonist and serotonin
17) Confidence 0.46 Published 2010 Journal Int. J. Neurosci. Section Abstract Doc Link 20504214 Disease Relevance 0.54 Pain Relevance 1.63
The results showed: (1) Pain stimulation increased norepinephrine (NE), but not epinephrine, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DA metabolic product), homovanilic acid (DA metabolic product), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HT metabolic product), acetycholine (Ach), choline (Ach metabolic product), gamma-aminobutyric acid (GABA), and L-glutamate acid concentrations in the PVN perfusion liquid; (2) PVN stimulation with L-glutamate sodium, which excited local neurons only, did not influence the concentrations of the studied classical neurotransmitter and metabolic product in the PVN perfusion liquid; (3) Microinjection of NE, epinephrine, or L-glutamate sodium into the PVN elevated pain threshold, and local administration of GABA decreased pain threshold in a dose-dependent manner, but PVN administration of Ach, DA, or 5-HT did not change pain threshold; (4) Microinjection of phentolamine (alpha-receptor antagonist) or MK801 [NMDA-receptor antagonist] into the PVN reduced pain threshold, and local administration of bicuculline (GABA-receptor antagonist) raised pain threshold, but PVN administration of propranolol (beta-receptor antagonist), atropine (Muscarinic cholinergic receptor antagonist), 6-OH gallamine (Nicotinic cholinergic receptor antagonist), fluperidol (DA-receptor antagonist), or cyproheptadine (5-HT-receptor antagonist) did not alter pain threshold.
Gene_expression (product) of Ach in neurons associated with pain, pain threshold, neurotransmitter, glutamate, gaba, dopamine, antagonist and serotonin
18) Confidence 0.46 Published 2010 Journal Int. J. Neurosci. Section Abstract Doc Link 20504214 Disease Relevance 0.54 Pain Relevance 1.63
In contrast, ACh produced an increase ( approximately 35%) in both AMPA/KA and NMDA receptor-mediated EPSCs when administered in the presence of the muscarinic antagonist atropine.
Gene_expression (produced) of ACh associated with antagonist and nmda receptor
19) Confidence 0.45 Published 2002 Journal J. Neurophysiol. Section Abstract Doc Link 12466449 Disease Relevance 0.06 Pain Relevance 0.31
The results showed that pain stimulation increased both AVP and Ach concentrations in the CdN perfusion liquid; AVP increased Ach concentration in the CdN perfusion liquid, while AVP receptor antagonist including d(CH(2))(5)Tyr(Me)AVP (V(1) receptor antagonist) and d(CH(2))(5)[D-Ile(2), Ile(4), Ala-NH(2)(9)]AVP (V(2) receptor antagonist) decreased Ach concentration in the CdN perfusion liquid.
Gene_expression (concentration) of Ach in CdN associated with pain and antagonist
20) Confidence 0.44 Published 2010 Journal Peptides Section Abstract Doc Link 19948196 Disease Relevance 0.39 Pain Relevance 0.67

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