INT209

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Context Info
Confidence 0.21
First Reported 1977
Last Reported 2010
Negated 1
Speculated 0
Reported most in Abstract
Documents 30
Total Number 30
Disease Relevance 2.54
Pain Relevance 16.31

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

cytosol (Pde5a) signal transduction (Pde5a)
Anatomy Link Frequency
pons 3
medulla 3
cerebellum 3
brain 2
striatum 1
Pde5a (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 90 99.56 Very High Very High Very High
midbrain 20 99.56 Very High Very High Very High
Morphine 40 99.52 Very High Very High Very High
tolerance 50 99.48 Very High Very High Very High
medulla 58 99.20 Very High Very High Very High
tetrodotoxin 32 98.84 Very High Very High Very High
Serotonin 102 98.82 Very High Very High Very High
GABAergic 135 98.80 Very High Very High Very High
depression 115 98.44 Very High Very High Very High
Spinal cord 50 98.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 37 99.82 Very High Very High Very High
Anxiety Disorder 50 98.92 Very High Very High Very High
Depression 115 98.44 Very High Very High Very High
Ganglion Cysts 27 95.44 Very High Very High Very High
Aggression 11 84.56 Quite High
Cognitive Disorder 197 76.12 Quite High
Graves' Ophthalmopathy 9 71.64 Quite High
Pressure Volume 2 Under Development 4 64.96 Quite High
Attention Deficit Hyperactivity Disorder 1 48.84 Quite Low
Increased Venous Pressure Under Development 38 28.72 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Unlike in the lizard neuromuscular junction, cannabinoids could depress transmission on their own but, in the presence of the cholinergic agonist, the NO–cGMP and cannabinoid pathways converged, apparently at the presynaptic location (where CB1 receptors and NO-evoked cGMP accumulation were located) to elicit the transient depression of GABAergic transmission.
Neg (NO) Positive_regulation (accumulation) of cGMP in neuromuscular junction associated with depression, gabaergic, cannabinoid and agonist
1) Confidence 0.21 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0.25 Pain Relevance 0.61
PDE inhibitors (PDE-Is) increase the intracellular amount of cAMP and/or cGMP by inhibiting the enzymatic degradation of these second messengers, dependent on the substrate specificity of the corresponding PDE (see also Table 2).
Positive_regulation (increase) of cGMP
2) Confidence 0.19 Published 2008 Journal Psychopharmacology (Berl) Section Body Doc Link PMC2704616 Disease Relevance 0.06 Pain Relevance 0
Concomitantly, anxiolytics including benzodiazepines reduced the stress-induced increase in central cGMP levels (Tang et al. 1997). cAMP levels were reduced as well after benzodiazepines administration, as found in vitro (Niles and Wang 1999); although increases in cAMP have also been observed (Cherry et al. 2001).
Positive_regulation (increase) of cGMP associated with stress and anxiety disorder
3) Confidence 0.18 Published 2008 Journal Psychopharmacology (Berl) Section Body Doc Link PMC2704616 Disease Relevance 0.80 Pain Relevance 0.06
Recent evidence indicates that phosphorylation by cAMP-dependent protein kinase enhances the associated guanylyl cyclase activity at resting levels of NO in pituitary cells (Kostic et al., 2004) whereas, in gastrointestinal smooth muscle cells, activation of muscarinic M2 receptors reduces cGMP generation through Src kinase-dependent tyrosine phosphorylation of the receptor (Murthy, 2008).
Positive_regulation (generation) of cGMP in smooth muscle cells
4) Confidence 0.16 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.08
Regarding the latter, recordings in the nucleus of the solitary tract found that, via cGMP, low concentrations of exogenous NO reversibly potentiated both glutamatergic EPSPs and GABAergic IPSPs, apparently through a presynaptic mechanism (Wang et al., 2007).
Positive_regulation (potentiated) of cGMP in nucleus associated with gabaergic
5) Confidence 0.15 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.35
m for cAMP), also contributes when cGMP reaches high levels (Bellamy & Garthwaite, 2001a); in ventrobasal thalamic neurones, on the other hand, PDE2 and putatively PDE9 appear most important (Hepp et al., 2007); PDE2 also plays a major role in hydrolyzing NO-evoked increases in cGMP levels in hippocampus and striatum (van Staveren et al., 2001; Wykes et al., 2002; Boess et al., 2004) whereas, in pituitary nerve terminals, PDE5 is again significant (Zhang et al., 2007b).
Positive_regulation (increases) of cGMP in hippocampus associated with hippocampus
6) Confidence 0.15 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0.07 Pain Relevance 0.05
In this respect there is a large literature dealing with NO–cGMP and Ca2+ homeostasis in cells of relevance to both its pre- and postsynaptic actions (reviewed in Garthwaite & Boulton, 1995; Clementi, 1998; Ahern et al., 2002; Grassi et al., 2004) but no general rules: in some cells Ca2+ currents are inhibited, in others they are enhanced; sometimes Ca2+ release from internal stores is reduced, elsewhere it is increased.
Positive_regulation (enhanced) of cGMP in internal
7) Confidence 0.15 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.45
Subsequent work extended this observation to provide a convincing case for NO serving as a retrograde messenger at these synapses in response to brief tetanic stimulation of the presynaptic neurone, and that it acts through cGMP and PKG (Arancio et al., 1995, 2001), leading to the rapid (within a minute) formation of new clusters of presynaptic proteins, coordinating with the slightly later appearance of new postsynaptic GluR1 clusters (Wang et al., 2005).
Positive_regulation (acts) of cGMP in synapses
8) Confidence 0.14 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.04
Alternatively, CNG channel activation following NO-evoked cGMP accumulation may produce excitatory postsynaptic responses in central neurones, as was shown first in a population of retinal ganglion cells (Ahmad et al., 1994; Kawa & Sterling, 2002) and, more recently, in medial vestibular nucleus neurones (Podda et al., 2008), but the engagement of this pathway by endogenous NO has not yet been demonstrated.
Positive_regulation (accumulation) of cGMP in medial vestibular nucleus associated with ganglion cysts
9) Confidence 0.14 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0.10 Pain Relevance 0
Further downstream, untangling the molecular mechanisms of short-term and long-term alterations occurring as a result of cGMP elevation, particularly when PKG activation is involved, will be challenging.
Positive_regulation (elevation) of cGMP
10) Confidence 0.14 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.10
Clonidine and both the (-)- and (+)-isomers of propranolol inhibited the stress-induced cGMP increase in a dose-related manner.
Positive_regulation (increase) of cGMP associated with stress and clonidine
11) Confidence 0.14 Published 1977 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 17881 Disease Relevance 0.35 Pain Relevance 0.35
Our results suggest that norepinephrine, serotonin, acetylcholine, or prostaglandins are not involved in the elevation of cGMP levels elicited by acute stress.
Positive_regulation (elevation) of cGMP associated with stress and serotonin
12) Confidence 0.14 Published 1977 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 17881 Disease Relevance 0.43 Pain Relevance 0.35
Acute stressing procedures cause a shortlasting increase in the levels of guanosie 3',5'-monophosphate (cGMP) in mouse brain without significantly influencing the concentrations of adenosine 3'-5'-monophosphate (cAMP).
Positive_regulation (increase) of cGMP in brain associated with adenocard
13) Confidence 0.14 Published 1977 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 17881 Disease Relevance 0.22 Pain Relevance 0.09
Abstinence caused increases in cGMP levels in corpus striatum (61%) and pons and medulla (45%).
Positive_regulation (increases) of cGMP in medulla associated with medulla
14) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.22
Abstinence from DPDPE produced increases in cGMP levels in pons and medulla (14%) but decreases in cerebellum (67%) and spinal cord (50%).
Positive_regulation (increases) of cGMP in cerebellum associated with medulla and spinal cord
15) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.39
Overall treatment with morphine and U-50,488H produced increases in cGMP levels in brain regions whereas DPDPE produced decreases in brain regions and spinal cord.
Positive_regulation (increases) of cGMP in brain associated with spinal cord and morphine
16) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.46
Tolerance to U-50,488H resulted in increases in cGMP levels in midbrain (52%) whereas abstinence from U-50,488H increased the cGMP levels in pons and medulla (76%).
Positive_regulation (increases) of cGMP in medulla associated with medulla, tolerance and midbrain
17) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.26
Tolerance to U-50,488H resulted in increases in cGMP levels in midbrain (52%) whereas abstinence from U-50,488H increased the cGMP levels in pons and medulla (76%).
Positive_regulation (increased) of cGMP in medulla associated with medulla, tolerance and midbrain
18) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.31
Tolerance to morphine was associated with highly significant increases in cGMP levels in corpus striatum (41%), cortex (36%), midbrain (73%) and cerebellum (51%) relative to controls.
Positive_regulation (increases) of cGMP in cerebellum associated with tolerance, midbrain and morphine
19) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.12
Tolerance to DPDPE was associated with increases in cGMP levels in hypothalamus (12%) and pons and medulla (33%) but decreases in cerebellum (66%) and spinal cord (58%).
Positive_regulation (increases) of cGMP in cerebellum associated with medulla, tolerance and spinal cord
20) Confidence 0.07 Published 1997 Journal Peptides Section Abstract Doc Link 9437726 Disease Relevance 0 Pain Relevance 1.34

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