INT7411

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Context Info
Confidence 0.78
First Reported 1986
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 40
Total Number 40
Disease Relevance 4.77
Pain Relevance 10.24

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

endoplasmic reticulum (FGFR3) cytoplasmic membrane-bounded vesicle (FGFR3) plasma membrane (FGFR3)
Anatomy Link Frequency
interneurons 4
neurons 2
prefrontal 1
blood 1
myocytes 1
FGFR3 (Homo sapiens)
Pain Link Frequency Relevance Heat
substance P 36 100.00 Very High Very High Very High
cocaine 12 99.84 Very High Very High Very High
Dopamine 9 99.80 Very High Very High Very High
tetrodotoxin 11 99.70 Very High Very High Very High
opiate 6 99.38 Very High Very High Very High
opioid receptor 6 99.28 Very High Very High Very High
Analgesic 22 99.20 Very High Very High Very High
Morphine 15 99.02 Very High Very High Very High
Enkephalin 293 98.82 Very High Very High Very High
GABAergic 36 98.68 Very High Very High Very High
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 8 98.64 Very High Very High Very High
INFLAMMATION 131 97.66 Very High Very High Very High
Cognitive Disorder 36 96.76 Very High Very High Very High
Bordatella Infection 4 95.72 Very High Very High Very High
Depression 124 92.12 High High
Rhinitis 126 89.76 High High
Inflammatory Bowel Disease 96 89.00 High High
Obesity 13 88.88 High High
Colitis 60 80.00 Quite High
Paralysis 13 79.36 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our study confirmed that the mechanism of action involves ACh release even if it is still unclear whether only muscarinic autoreceptors or, also, heteroreceptors are involved.
Localization (release) of ACh
1) Confidence 0.78 Published 1994 Journal J. Med. Chem. Section Abstract Doc Link 8201605 Disease Relevance 0.25 Pain Relevance 0.51
Since the enhancement of central cholinergic transmission could be beneficial for cognitive disorders, we manipulated (R)-(+)-hyoscyamine, synthesizing several derivatives of tropic and 2-phenylpropionic acids, with the aim of obtaining drugs which are able to increase ACh release and consequently to show analgesic and nootropic activities.
Localization (release) of ACh associated with cognitive disorder and analgesic
2) Confidence 0.68 Published 1994 Journal J. Med. Chem. Section Abstract Doc Link 8201605 Disease Relevance 0.25 Pain Relevance 0.52
This experiment investigated the influence of age on prefrontal acetylcholine (ACh) release and Fos response in the hypothalamic paraventricular nucleus and the nucleus tractus solitarius (NTS) of rats following isoflurane anesthesia.
Localization (release) of ACh in prefrontal associated with anesthesia and isoflurane
3) Confidence 0.68 Published 2004 Journal Exp. Neurol. Section Abstract Doc Link 15530892 Disease Relevance 0 Pain Relevance 0.32
delta 1-Opioid receptor-mediated control of acetylcholine (ACh) release in human neocortex slices.
Localization (release) of ACh in neocortex associated with enkephalin and opioid receptor
4) Confidence 0.68 Published 1998 Journal Int. J. Dev. Neurosci. Section Title Doc Link 10198826 Disease Relevance 0 Pain Relevance 0.80
Previous studies have shown that (R)-(+)-hyoscyamine has analgesic activity as a consequence of increased ACh release following antagonism of central muscarinic autoreceptors.
Localization (release) of ACh associated with analgesic
5) Confidence 0.68 Published 1994 Journal J. Med. Chem. Section Abstract Doc Link 8201605 Disease Relevance 0.22 Pain Relevance 0.43
To determine if phenytoin reduces depolarization-linked acetylcholine release from synaptosomes solely by interacting with Na+, the effect of phenytoin (100 to 200 microM) and/or tetrodotoxin (1 microM) on ACh release was assayed in synaptosomes depolarized with either KCl 56 mM or veratridine 10 microM.
Localization (release) of ACh associated with tetrodotoxin
6) Confidence 0.68 Published 1986 Journal Exp. Neurol. Section Abstract Doc Link 3780920 Disease Relevance 0 Pain Relevance 0.32
Morphine stimulates opiate kappa receptors and depresses ACh release.
Localization (release) of ACh associated with opiate and morphine
7) Confidence 0.61 Published 1991 Journal Reprod. Fertil. Dev. Section Abstract Doc Link 1957023 Disease Relevance 0.23 Pain Relevance 0.70
Studies described in this paper, performed on electrically stimulated striatal slices and on cholinergic cell lines, test this hypothesis. 1) Electrically-stimulated striatal slices continue to release ACh, and sustain their free choline and ACh levels, even when perfused with a choline-free medium.
Localization (release) of ACh
8) Confidence 0.59 Published 1987 Journal J. Neural Transm. Suppl. Section Abstract Doc Link 3316498 Disease Relevance 0.13 Pain Relevance 0.13
After the release of ACh, three complexes are formed between ACh and the receptors: ARO, ORA, and ARA.
Localization (release) of ACh
9) Confidence 0.58 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0 Pain Relevance 0
The simulations are based on the postulate by Bowman [7] that twitch fade is due to the decreased amount of ACh released by the fourth stimulus as compared to that released by the first stimulus.
Localization (released) of ACh
10) Confidence 0.55 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0.18 Pain Relevance 0.09
Cocaine blocks Ca2+ influx and thus blocks ACh release.
Localization (release) of ACh associated with cocaine
11) Confidence 0.53 Published 1991 Journal Reprod. Fertil. Dev. Section Abstract Doc Link 1957023 Disease Relevance 0.28 Pain Relevance 0.71
By interfering with ACh release and placental blood flow, the three drugs of abuse may depress the diffusion of amino acids and other nutrients from the trophoblast into the placental circulation.
Localization (release) of ACh in blood
12) Confidence 0.53 Published 1991 Journal Reprod. Fertil. Dev. Section Abstract Doc Link 1957023 Disease Relevance 0.33 Pain Relevance 0.66
The doses of vecuronium used in this study decrease the amount of ACh released by the fourth stimulus up to about 70% of the amount released by the first stimulus.
Localization (released) of ACh
13) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0 Pain Relevance 0
The simulated result that no fade is present if the amount of ACh released by the fourth stimulus remains identical to that released by the first stimulus, i.e. if [A]4 = [A]1 (Figure 3), contradicts the suggestion that, even in the absence of neuromuscular blocking drugs, a spontaneous fall-off of the ACh quantal content occurs at 2 Hz stimulation frequency [18].
Localization (released) of ACh
14) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0 Pain Relevance 0
The correlation between the clinically observed fade and the simulated decrease in [A]4/[A]1 allowed us to suggest tentative estimates for the vecuronium-induced decrease of ACh release elicited by the fourth stimulus during the TOF pattern of stimulation.
Localization (release) of ACh
15) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0.05 Pain Relevance 0.03
The number of ACh molecules released by the first stimulus was postulated to establish a constant initial concentration of ACh, [A]1 = 7.75 × 10-6 M.
Localization (released) of ACh
16) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0.07 Pain Relevance 0.03
The primary purpose of the present study was to correlate twitch fade, as observed in the current study and by the other investigators, with the decrease in ACh release that would be necessary to produce the fade.
Localization (release) of ACh
17) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0.20 Pain Relevance 0.10
The concentrations of all three complexes increase transiently after the release of ACh, reach a peak, and subsequently decline due to hydrolysis of free ACh.
Localization (release) of ACh
18) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0 Pain Relevance 0
The model considers the stimulus-induced release of ACh into a synaptic cleft, ACh binding to two sites at a single postsynaptic receptor, and ACh hydrolysis.
Localization (release) of ACh in synaptic cleft
19) Confidence 0.51 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0.07 Pain Relevance 0.04
If the fourth stimulus releases the same number of ACh molecules as does the first, i.e. if [A]4/[A]1 = 1, then T4 remains equal to T1, i.e.
Localization (releases) of ACh
20) Confidence 0.45 Published 2007 Journal Theor Biol Med Model Section Body Doc Link PMC1939837 Disease Relevance 0 Pain Relevance 0

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