INT1352

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Context Info
Confidence 0.80
First Reported 1976
Last Reported 2010
Negated 2
Speculated 6
Reported most in Abstract
Documents 728
Total Number 735
Disease Relevance 73.01
Pain Relevance 296.01

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 45
hippocampus 43
brain 23
nerve 19
cortex 18
Acot1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 711 100.00 Very High Very High Very High
gABA 277 100.00 Very High Very High Very High
Neurotransmitter 238 100.00 Very High Very High Very High
Catecholamine 73 100.00 Very High Very High Very High
Calcitonin gene-related peptide 36 100.00 Very High Very High Very High
Cholecystokinin 33 100.00 Very High Very High Very High
tetrodotoxin 580 99.92 Very High Very High Very High
Morphine 470 99.92 Very High Very High Very High
Somatostatin 398 99.92 Very High Very High Very High
fluoxetine 80 99.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 223 100.00 Very High Very High Very High
Urological Neuroanatomy 240 99.98 Very High Very High Very High
Porphyria 36 99.84 Very High Very High Very High
Hyperglycemia 30 99.84 Very High Very High Very High
Pressure Volume 2 Under Development 7 99.82 Very High Very High Very High
Alzheimer's Dementia 74 99.78 Very High Very High Very High
INFLAMMATION 544 99.76 Very High Very High Very High
Ganglion Cysts 64 99.74 Very High Very High Very High
Opiate Addiction 60 99.72 Very High Very High Very High
Pain 89 99.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Using in vivo microdialysis, the releases of Ach and Ch, functional parameters of cholinergic system, were determined in freely moving rats.
Localization (releases) of Ach
1) Confidence 0.80 Published 2009 Journal Zhonghua Yi Xue Za Zhi Section Body Doc Link 20095350 Disease Relevance 0.09 Pain Relevance 0
In the experiment group, the hippocampal releases of Ach and Ch were markedly different between cognition markedly impaired group and cognition lightly impaired group.
Localization (releases) of Ach
2) Confidence 0.80 Published 2009 Journal Zhonghua Yi Xue Za Zhi Section Body Doc Link 20095350 Disease Relevance 0.06 Pain Relevance 0
Results indicate that Novelty, but not Formalin or Restraint, increases ACh release in the hippocampus and that the type of behavioral state displayed by the animal at the time of formalin injection determines the response of the septo-hippocampal cholinergic pathway.
Localization (release) of ACh in hippocampus associated with hippocampus
3) Confidence 0.80 Published 1997 Journal Brain Res. Section Abstract Doc Link 9067465 Disease Relevance 0.27 Pain Relevance 0.22
Ovariectomy caused the significant increase in both TTX-insensitive basal Ach release and TTX-insensitive stretch-induced Ach release.
Localization (release) of Ach
4) Confidence 0.79 Published 2007 Journal Neurourol. Urodyn. Section Body Doc Link 17480029 Disease Relevance 0.14 Pain Relevance 0
The fenfluramine's ability to increase ACh release was potentiated by E(2) replacement with a 0.5 mg-pellet.
Localization (release) of ACh
5) Confidence 0.77 Published 2002 Journal Brain Res. Section Abstract Doc Link 12020863 Disease Relevance 0.39 Pain Relevance 0.23
The selective micro-opiate agonist, [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (1 microM, coapplied with NMDA), was without effect on the NMDA-evoked release of ACh but abolished both dopamine-dependent (morning) and dopamine-independent (afternoon) responses of beta-funaltrexamine (10 nM and 1 microM).Therefore, in the limbic territory of the striatum enriched in striosomes, the micro-opioid-inhibitory regulation of ACh release follows diurnal rhythms.
Localization (release) of ACh in striatum associated with dopamine, agonist, enkephalin, opiate and opioid
6) Confidence 0.77 Published 2004 Journal Neuroscience Section Abstract Doc Link 14706785 Disease Relevance 0 Pain Relevance 0.73
Both basal and stimulated ACh release were found to be tetrodotoxin (TTX) sensitive.
Localization (release) of ACh associated with tetrodotoxin
7) Confidence 0.76 Published 1993 Journal Brain Res. Section Abstract Doc Link 8111630 Disease Relevance 0 Pain Relevance 0.19
Ch administration significantly increased ACh release (to 136% of basal values; P < 0.01) in the presence of the low neostigmine concentration, but failed to significantly increase ACh release following local electrical depolarization of striatal neurons.
Localization (release) of ACh in neurons
8) Confidence 0.76 Published 1993 Journal Brain Res. Section Abstract Doc Link 8111630 Disease Relevance 0 Pain Relevance 0.19
Robust FLU-mediated inhibition of ACh release was evident in slices from pCOC male and pCOC diestrus female rats vs. their respective PSAL control groups.
Localization (release) of ACh associated with fluoxetine
9) Confidence 0.73 Published 2002 Journal Prog. Neuropsychopharmacol. Biol. Psychiatry Section Abstract Doc Link 12502023 Disease Relevance 0 Pain Relevance 0.90
During the later phase of abstinence, when no withdrawal symptoms were detectable, the opposite effect, i.e. an increase of ACh release was found.
Localization (release) of ACh associated with withdrawal
10) Confidence 0.71 Published 1999 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 10102787 Disease Relevance 0.19 Pain Relevance 0.96
On Day 2, ACh release increased in both sexes during the Formalin test.
Localization (release) of ACh
11) Confidence 0.71 Published 1999 Journal Brain Res. Section Abstract Doc Link 9878722 Disease Relevance 0.22 Pain Relevance 0.29
In a separate experiment, ACh release in the NAC was monitored in 10-min intervals during free-feeding; ACh increased in the interval immediately following maximal food intake.
Localization (release) of ACh in NAC associated with nucleus accumbens
12) Confidence 0.70 Published 1992 Journal J. Neurochem. Section Abstract Doc Link 1573406 Disease Relevance 0 Pain Relevance 0.63
Morphine at a low dose of 5 mg/kg (i.p.) increased ACh release by the RVLM by 42.4%.
Localization (release) of ACh in RVLM associated with rostral ventrolateral medulla and morphine
13) Confidence 0.70 Published 1999 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 10336550 Disease Relevance 0 Pain Relevance 1.08
In accordance with an involvement of the 5-HT1B receptor in the ACh facilitation induced by d-norfenfluramine is the finding that the selective 5-HT1B agonist, CP-93,129, given locally (2, 4 and 8 micrograms/side) does-dependently raised cortical ACh release.
Localization (release) of ACh associated with agonist
14) Confidence 0.70 Published 1996 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 8627564 Disease Relevance 0.38 Pain Relevance 0.27
Unlike ACh release, DA release showed no frequency dependence above 5 Hz.
Localization (release) of ACh associated with addiction and dopamine
15) Confidence 0.70 Published 1993 Journal Brain Res. Section Abstract Doc Link 8481795 Disease Relevance 0 Pain Relevance 0.44
Phenobarbital inhibited the K-stimulated [3H]ACh release and the IC50 was equal to that found for K-stimulated endogenous ACh release.
Localization (release) of ACh
16) Confidence 0.70 Published 1980 Journal Neurochem. Res. Section Abstract Doc Link 6968410 Disease Relevance 0 Pain Relevance 0.15
Peripheral administration of choline (Ch) chloride (30-120 mg/kg) to anesthetized animals caused dose-related (r = 0.994, P < 0.01) increases in ACh release; basal release rose from 117 +/- 7% to 141 +/- 5% of initial baseline levels (P < 0.05) and electrically evoked ACh release rose from 386 +/- 38% to 600 +/- 34% (P < 0.01) in rats given 120 mg/kg.
Localization (release) of ACh
17) Confidence 0.70 Published 1993 Journal Brain Res. Section Abstract Doc Link 8481795 Disease Relevance 0 Pain Relevance 0.44
Moreover, oxotremorine, but not pilocarpine, inhibited ACh release in a concentration-dependent manner in either basal- or picric acid-evoked conditions, indicating the presence of muscarinic M2-receptors for auto-regulation of ACh release.
Localization (release) of ACh
18) Confidence 0.70 Published 1986 Journal Neurosci. Lett. Section Abstract Doc Link 2875422 Disease Relevance 0 Pain Relevance 0.23
Moreover, oxotremorine, but not pilocarpine, inhibited ACh release in a concentration-dependent manner in either basal- or picric acid-evoked conditions, indicating the presence of muscarinic M2-receptors for auto-regulation of ACh release.
Localization (release) of ACh
19) Confidence 0.70 Published 1986 Journal Neurosci. Lett. Section Abstract Doc Link 2875422 Disease Relevance 0 Pain Relevance 0.23
These results suggest that cyclic GMP may mediate the regulation of ACh release by presynaptic muscarinic receptors.
Localization (release) of ACh
20) Confidence 0.70 Published 1980 Journal Brain Res. Section Abstract Doc Link 6243230 Disease Relevance 0 Pain Relevance 0.09

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