INT45437

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Context Info
Confidence 0.79
First Reported 1984
Last Reported 2010
Negated 3
Speculated 1
Reported most in Abstract
Documents 84
Total Number 86
Disease Relevance 17.37
Pain Relevance 22.18

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 10
cortex 6
vesicles 5
motor nerve 4
motor neurons 3
Acot1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 153 100.00 Very High Very High Very High
cytokine 42 100.00 Very High Very High Very High
calcitonin gene related peptide 80 99.80 Very High Very High Very High
substance P 46 99.80 Very High Very High Very High
dorsal root ganglion 72 99.76 Very High Very High Very High
Serotonin 268 99.72 Very High Very High Very High
isoflurane 37 99.68 Very High Very High Very High
Potency 13 99.68 Very High Very High Very High
cINOD 8 99.66 Very High Very High Very High
Spinal cord 63 99.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 159 100.00 Very High Very High Very High
Syndrome 102 99.84 Very High Very High Very High
Nociception 54 99.78 Very High Very High Very High
Ganglion Cysts 121 99.76 Very High Very High Very High
Targeted Disruption 190 99.52 Very High Very High Very High
Paralysis 10 99.28 Very High Very High Very High
Occupational Lung Diseases 56 98.76 Very High Very High Very High
Sprains And Strains 48 98.72 Very High Very High Very High
Asthma 230 94.28 High High
Disease 354 92.56 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These data support the conclusion that ACh release in PnO of B6 mouse is modulated by non-M1 muscarinic receptors.
Localization (release) of ACh
1) Confidence 0.79 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.32
These are the first neurochemical data showing that ACh release in the pontine reticular formation of the B6 mouse is modulated by NO.
Localization (release) of ACh in reticular formation
2) Confidence 0.77 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.06
Isoflurane and halothane anesthesia have been shown to decrease ACh release in the medial pontine reticular formation.
Localization (release) of ACh in medial associated with anesthesia, halothane and isoflurane
3) Confidence 0.68 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.47
Nitric oxide (NO)-releasing beads microinjected into the pontine reticular formation of C57BL/6J (B6) mice significantly (P < 0.0001) increased ACh release.
Localization (release) of ACh in reticular formation
4) Confidence 0.68 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0
Therefore, an additional series of studies quantified the effects of a soluble guanylate cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), on ACh release in the cat medial pontine reticular formation.
Localization (release) of ACh in reticular formation
5) Confidence 0.68 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.34
During naturally occurring states of sleep and wakefulness, but not anesthesia, ODQ caused a significant (P < 0.001) decrease in ACh release.
Localization (release) of ACh associated with anesthesia
6) Confidence 0.68 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.41
Both high K+ and veratridine, depolarizing agents with different mechanisms of action, lowered the ACh content of the cytoplasmic (S3) fraction of mouse forebrain minces incubated in a Ca2+-free Krebs solution, without stimulating ACh release or altering the level of ACh in the vesicle-bound (P3) fraction.
Localization (release) of ACh in vesicle
7) Confidence 0.67 Published 1984 Journal Brain Res. Section Abstract Doc Link 6697191 Disease Relevance 0 Pain Relevance 0.08
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.
Localization (release) of ACh in cortex
8) Confidence 0.66 Published 2002 Journal J. Neurophysiol. Section Abstract Doc Link 12037184 Disease Relevance 0 Pain Relevance 0.17
This hypothesis was evaluated using microdialysis delivery of the muscarinic antagonist AF-DX116 (3 nM) while simultaneously quantifying ACh release in prefrontal cortex, number of 7- to 14-Hz EEG spindles, and EEG power spectral density.
Localization (release) of ACh in cortex associated with antagonist
9) Confidence 0.66 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).
Localization (release) of ACh associated with antagonist and potency
10) Confidence 0.60 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.34
The mouse is recognized as a powerful model for pharmacogenomics but the synaptic mechanisms regulating ACh release in mouse pontine reticular formation have not been characterized.
Localization (release) of ACh in reticular formation
11) Confidence 0.60 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.21
Drug delivery by microdialysis was used in isoflurane-anesthetized C57BL/6J (B6) mice (n=33) to test the hypothesis that muscarinic autoreceptors modulate ACh release in the pontine reticular nucleus, oral part (PnO).
Localization (release) of ACh in nucleus associated with isoflurane
12) Confidence 0.60 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.32
The muscarinic agonist bethanechol dialyzed into the PnO significantly decreased ACh release by 60% compared with control.
Localization (release) of ACh associated with agonist
13) Confidence 0.60 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.36
The muscarinic antagonist scopolamine increased ACh release in the PnO by 21% (3 nM), 48% (10 nM), 56% (30 nM), and 104% (100 nM).
Localization (release) of ACh associated with antagonist
14) Confidence 0.60 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207318 Disease Relevance 0 Pain Relevance 0.36
These results suggest that endogenous ACh in the spinal cord acts as a transmitter anti-nociception, and that ACh release regulated by presynaptic M(3) muscarinic receptors in the spinal cord is involved in the second phase of nociception induced by formalin.
Localization (release) of ACh in spinal cord associated with nociception and spinal cord
15) Confidence 0.59 Published 2000 Journal Brain Res. Section Abstract Doc Link 10720613 Disease Relevance 0.44 Pain Relevance 0.35
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).
Localization (release) of ACh in reticular formation
16) Confidence 0.59 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.05
ACh regulates arousal, and the present study was designed to provide insight into the neurochemical mechanisms modulating ACh release in the pontine reticular formation.
Localization (release) of ACh in reticular formation
17) Confidence 0.59 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0
Considered together, results from the mouse and cat indicate that NO modulates ACh release in arousal-promoting regions of the pontine reticular formation via an NO-sensitive sGC-cGMP pathway.
Neg (NO) Localization (release) of ACh in reticular formation
18) Confidence 0.59 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.44
The signal transduction cascade through which NO modulates ACh release in the pontine reticular formation has not previously been characterized.
Localization (release) of ACh in reticular formation
19) Confidence 0.59 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.10
The finding that ODQ did not alter ACh release during isoflurane or halothane anesthesia demonstrates that these anesthetics disrupt the NO-sensitive sGC-cGMP pathway.
Localization (release) of ACh associated with anesthesia, halothane and isoflurane
20) Confidence 0.59 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.47

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