INT354040

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Context Info
Confidence 0.76
First Reported 2011
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 3.65
Pain Relevance 0.58

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

signal transduction (Avpr1b) plasma membrane (Avpr1b) response to stress (Avpr1b)
signal transducer activity (Avpr1b)
Anatomy Link Frequency
corticotrophs 2
pancreatic islets 1
blood 1
pancreas 1
Avpr1b (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 54 99.50 Very High Very High Very High
antagonist 102 96.32 Very High Very High Very High
Hyperalgesia 6 34.56 Quite Low
amygdala 6 17.20 Low Low
Hippocampus 24 13.52 Low Low
Pyramidal cell 6 12.44 Low Low
antidepressant 6 11.04 Low Low
Potency 12 9.44 Low Low
depression 48 5.00 Very Low Very Low Very Low
medulla 36 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 480 98.92 Very High Very High Very High
Targeted Disruption 360 98.70 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 12 94.44 High High
Sprains And Strains 72 83.84 Quite High
Obesity 18 65.24 Quite High
Affective Disorder 12 53.04 Quite High
Diabetes Mellitus 6 44.72 Quite Low
Hyperalgesia 6 34.56 Quite Low
Aggression 102 26.24 Quite Low
Depression 60 21.04 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As Oxt at high concentrations can elicit ACTH release via the Avpr1b, and the Oxtr may be expressed in corticotrophs, it has been suggested that increased expression of Oxtrs may be a compensatory mechanism through which Avpr1b KO mice and Brattleboro rats can, to some degree, make up for the lack of Avpr1b/Avp-mediated ACTH release (Nakamura et al. 2008).
Localization (release) of Avpr1b in corticotrophs associated with targeted disruption
1) Confidence 0.76 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 0.62 Pain Relevance 0
As Oxt at high concentrations can elicit ACTH release via the Avpr1b, and the Oxtr may be expressed in corticotrophs, it has been suggested that increased expression of Oxtrs may be a compensatory mechanism through which Avpr1b KO mice and Brattleboro rats can, to some degree, make up for the lack of Avpr1b/Avp-mediated ACTH release (Nakamura et al. 2008).
Localization (release) of Avpr1b in corticotrophs associated with targeted disruption
2) Confidence 0.71 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 0.86 Pain Relevance 0.03
While Avp acts on the Avpr1b to decrease blood sugar levels through insulin release, it can also act in opposition to this by stimulating glucagon release (Yibchok-anun and Hsu 1998) and promoting hepatic glycogenolysis (Kirk et al. 1979).
Localization (decrease) of Avpr1b in blood
3) Confidence 0.71 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 0.15 Pain Relevance 0
This may be an important consideration, as Oxtrs in addition to Avpr1bs are apparently present in pancreatic islets (Oshikawa et al. 2004) and have been shown to cause insulin/glucagon release (Jeng et al. 1996; Yibchok-anun et al. 1999).
Localization (release) of Avpr1bs in pancreatic islets
4) Confidence 0.71 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 0.06 Pain Relevance 0.14
One such member of the recent modified range of Avp analogue agonists, d[Leu4,Lys8] Avp, is noted to be a full agonist at human, rat and mouse Avpr1bs in vitro as well as stimulates ACTH and insulin release at low doses from mouse pituitary and perfused rat pancreas, respectively (Pena et al. 2007b).
Localization (release) of Avpr1bs in pancreas associated with agonist
5) Confidence 0.71 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 0.11 Pain Relevance 0.36
The studies in Avpr1b KO mice and Brattleboro rats highlight the discrepancy between Avp/Avpr1b-mediated ACTH and CORT secretion during acute and repeated stress—this may have implications on the potential use of Avpr1b antagonists to ameliorate symptoms of HPA axis hyperactivity in stress-related disorders.


Localization (secretion) of Avpr1b associated with stress, targeted disruption, antagonist and attention deficit hyperactivity disorder
6) Confidence 0.66 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 1.84 Pain Relevance 0.05

General Comments

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