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Context Info
Confidence 0.30
First Reported 2000
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 0.93
Pain Relevance 1.59

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

extracellular space (Srgn) extracellular region (Srgn) Golgi apparatus (Srgn)
Anatomy Link Frequency
reticular formation 2
neurons 1
spinal cord 1
Srgn (Mus musculus)
Pain Link Frequency Relevance Heat
Neuronal nitric oxide synthase 1 100.00 Very High Very High Very High
Spinal cord 35 99.08 Very High Very High Very High
anesthesia 6 94.04 High High
halothane 4 93.60 High High
isoflurane 4 93.08 High High
Eae 7 90.28 High High
Pain 31 89.92 High High
allodynia 10 82.24 Quite High
Morphine 16 73.60 Quite High
Analgesic 3 73.24 Quite High
Disease Link Frequency Relevance Heat
Inflammatory Pain 4 90.28 High High
Pain 43 89.92 High High
Neuropathic Pain 15 82.24 Quite High
Hypoxia 3 80.76 Quite High
Nociception 40 79.92 Quite High
Shock 8 76.64 Quite High
Targeted Disruption 33 30.08 Quite Low
Sprains And Strains 47 25.96 Quite Low
Infection 37 5.00 Very Low Very Low Very Low
Malaria 31 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
Regulation (modulates) of sGC in reticular formation
1) Confidence 0.30 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.44
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.
Regulation (effects) of sGC in reticular formation
2) Confidence 0.30 Published 2006 Journal J. Appl. Physiol. Section Abstract Doc Link 16424074 Disease Relevance 0 Pain Relevance 0.26
Conventional sGCs are potently activated by the gaseous messenger, nitric oxide (NO) whereas atypical sGCs are poorly regulated by NO.
Regulation (regulated) of sGC
3) Confidence 0.26 Published 2006 Journal Journal of Insect Science Section Body Doc Link PMC2990333 Disease Relevance 0.23 Pain Relevance 0
The localization and regulation of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and soluble guanylyl cyclase (sGC) were assessed in the spinal cord of mice stimulated by an intraplantar injection of zymosan.
Regulation (regulation) of sGC in spinal cord associated with spinal cord and neuronal nitric oxide synthase
4) Confidence 0.20 Published 2000 Journal Neurosci. Lett. Section Abstract Doc Link 10925177 Disease Relevance 0.15 Pain Relevance 0.18
Previously provided pharmacological evidence demonstrates the participation of HO [2,3], NOS [14,15], sGC [7] and PKG [8,9] in at least the acute phases of formalin stimulation.
Regulation (participation) of sGC
5) Confidence 0.06 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.55 Pain Relevance 0.61
Soluble guanylyl cyclase (sGC), a well-characterized molecular target of NO which causes an increase in intracellular cGMP in many cell types [4], is not expressed in DRG neurons [24].
Regulation (target) of sGC in neurons
6) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2764051 Disease Relevance 0 Pain Relevance 0.10

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