INT8781

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.45
First Reported 1989
Last Reported 2010
Negated 2
Speculated 1
Reported most in Abstract
Documents 6
Total Number 6
Disease Relevance 0.67
Pain Relevance 3.58

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

extracellular region (Prlh) lipid metabolic process (Prlh) cytoplasm (Prlh)
Anatomy Link Frequency
nucleus 3
neurons 1
body 1
Prlh (Rattus norvegicus)
Pain Link Frequency Relevance Heat
medulla 6 100.00 Very High Very High Very High
Somatostatin 5 100.00 Very High Very High Very High
Locus ceruleus 28 99.68 Very High Very High Very High
Cholecystokinin 2 99.48 Very High Very High Very High
substance P 5 99.04 Very High Very High Very High
Enkephalin 12 98.54 Very High Very High Very High
lidocaine 3 97.92 Very High Very High Very High
Pain 3 97.46 Very High Very High Very High
Neuropeptide 4 96.44 Very High Very High Very High
Nicotine 4 96.40 Very High Very High Very High
Disease Link Frequency Relevance Heat
Body Weight 4 100.00 Very High Very High Very High
Pain 7 97.46 Very High Very High Very High
Cognitive Disorder 19 95.92 Very High Very High Very High
Neurological Disease 1 71.32 Quite High
Injury 1 5.00 Very Low Very Low Very Low
Frailty 1 5.00 Very Low Very Low Very Low
Peripheral Arterial Disease 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the present study this effect of nicotine was attenuated (to about 25% of control response) by injection of lidocaine into the nucleus paragigantocellularis (PGi) whereas injection into the nucleus prepositus hypoglossi (PrH) had no effect in this regard.
Neg (no) Regulation (effect) of PrH in nucleus associated with nicotine and lidocaine
1) Confidence 0.45 Published 1989 Journal Neurosci. Lett. Section Abstract Doc Link 2771156 Disease Relevance 0 Pain Relevance 0.67
Recent anatomic studies in our laboratory (Aston-Jones et al., 1986) identified the nucleus prepositus hypoglossi (PrH) in the dorsomedial medulla as a major afferent of the locus coeruleus (LC).
Regulation (afferent) of PrH in nucleus associated with medulla and locus ceruleus
2) Confidence 0.44 Published 1989 Journal J. Neurosci. Section Abstract Doc Link 2769374 Disease Relevance 0 Pain Relevance 0.63
Overall, 57% and 56% of the LC-projecting neurons in PGi and PrH, respectively, were also immunoreactive for ENK, suggesting that enkephalinergic neurons of PGi and PrH are major afferents to noradrenergic LC neurons.
Regulation (afferents) of PrH in neurons associated with locus ceruleus
3) Confidence 0.43 Published 1992 Journal J. Neurosci. Section Abstract Doc Link 1379635 Disease Relevance 0 Pain Relevance 0.52
The results showed that (1) intraventricular injection (icv) of anti-arginine vasopressin (AVP) serum completely reversed pain threshold increase induced by l-glutamate sodium (Glu) injection into the PVN, and local administration (icv) of anti-leucine-enkephalin (L-Ek) serum or anti-beta-endorphin (beta-Ep) serum partly attenuated pain threshold increase induced by Glu injection into the PVN, but pre-treatment of anti-oxytocin (OXT), dynorphinA(1-13) (DynA(1-13)), cholecystokinin-like peptide (CCK), neurotensin (NT), corticotrophin-releasing hormone (CRH), adrenocorticotrophin (ACTH), somatostatin (SST), prolactin-releasing hormone (PRH), angiotensinII (AngII), vasoactive intestinal polypeptide (VIP), melanotropin-releasing hormone (MRH), thyrotropin-releasing hormone (TRH), substance P (SP) or growth hormone-releasing hormone (GHRH) serum (icv) did not influence the analgesic effect of PVN administration with Glu; (2) PVN stimulation with Glu elevated the concentrations of AVP, OXT, CCK, NT, CRH, SST, PRH and DynA(1-13) in PVN perfusion liquid, and could not change the concentrations of L-Ek, beta-Ep, AngII, ACTH, VIP, MRH, TRH, SP and GHRH in PVN perfusion liquid; (3) Pain stimulation increased the concentrations of AVP, L-Ek, beta-Ep, DynA(1-13), CRH and ACTH in PVN perfusion liquid, and did not alter the concentrations of OXT, CCK, NT, SST, PRH, AngII, VIP, MRH, TRH, SP and GHRH in PVN perfusion liquid.
Neg (not) Regulation (alter) of PRH in PVN associated with pain, glutamate, pain threshold, analgesic, somatostatin, enkephalin, cholecystokinin and substance p
4) Confidence 0.24 Published 2007 Journal Neuropeptides Section Abstract Doc Link 17316791 Disease Relevance 0.25 Pain Relevance 1.40
Here, there was no group or session effect (both Fs < 1), although there was a small, but nonsignificant, difference in profiles, Group × Session interaction, F(1, 11) = 4.20, p = .065, as the PRh group seemed less affected by the change in stimulus pairings.


Spec (seemed) Regulation (affected) of PRh
5) Confidence 0.22 Published 2010 Journal Behav Neurosci Section Body Doc Link PMC2834571 Disease Relevance 0.10 Pain Relevance 0
In this overview, an introduction to the GPCRs and the field of central regulation of food intake is provided together with brief mentioning of some other GPCRs that are also implicated in regulation of body weight, such as the melanin-concentrating hormone (MCH), neuromedin U, prolactin-releasing peptide (PrRP), bombesin, cholecystokinin (CCK), Glucagon-like peptide-1 (GLP-1) (and oxyntomodulin), neuropeptide B (NPB) and neuropeptide W (NPW), opioids peptides, free fatty acid (FFA) receptors (GPR40, GPR41).
Regulation (regulation) of PrRP in body associated with body weight, neuropeptide, opioid and cholecystokinin
6) Confidence 0.03 Published 2006 Journal CNS Neurol Disord Drug Targets Section Abstract Doc Link 16787226 Disease Relevance 0.32 Pain Relevance 0.37

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox