An investigation into the noradrenergic and serotonergic contributions of diffuse noxious inhibitory controls in a monoiodoacetate model of osteoarthritis.
Action Potentials
/ drug effects
Adrenergic alpha-2 Receptor Antagonists
/ pharmacology
Animals
Diffuse Noxious Inhibitory Control
/ drug effects
Disease Models, Animal
Disease Progression
Ganglia, Spinal
/ drug effects
Iodoacetic Acid
Male
Neural Inhibition
/ drug effects
Neurons
/ drug effects
Norepinephrine
/ metabolism
Osteoarthritis
/ metabolism
RNA, Messenger
/ metabolism
Rats, Sprague-Dawley
Receptors, Adrenergic, alpha-2
/ metabolism
Receptors, Serotonin
/ metabolism
Serotonin
/ metabolism
Serotonin Antagonists
/ pharmacology
Spinal Cord
/ drug effects
descending modulation
diffuse noxious inhibitory controls
norepinephrine
serotonin
Journal
Journal of neurophysiology
ISSN: 1522-1598
Titre abrégé: J Neurophysiol
Pays: United States
ID NLM: 0375404
Informations de publication
Date de publication:
01 01 2019
01 01 2019
Historique:
pubmed:
22
11
2018
medline:
23
8
2019
entrez:
22
11
2018
Statut:
ppublish
Résumé
Osteoarthritis (OA) is a debilitating conditioning with pain as the major clinical symptom. Understanding the mechanisms that drive OA-associated chronic pain is crucial for developing the most effective analgesics. Although the degradation of the joint is the initial trigger for the development of chronic pain, the discordance between radiographic joint damage and the reported pain experience in patients, coupled with clinical features that cannot be explained by purely peripheral mechanisms, suggest there are often other factors at play. Therefore, this study considers the central contributions of chronic pain, using a monoiodoacetate (MIA) model of OA. Particularly, this study explores the functionality of descending controls over the course of the model by assessing diffuse noxious inhibitory controls (DNIC). Early-phase MIA animals have a functional DNIC system, whereas DNIC are abolished in late-phase MIA animals, indicating a dysregulation in descending modulation over the course of the model. In early-phase animals, blocking the actions of spinal α
Identifiants
pubmed: 30461363
doi: 10.1152/jn.00613.2018
pmc: PMC6383660
doi:
Substances chimiques
Adrenergic alpha-2 Receptor Antagonists
0
RNA, Messenger
0
Receptors, Adrenergic, alpha-2
0
Receptors, Serotonin
0
Serotonin Antagonists
0
serotonin 7 receptor
0
Serotonin
333DO1RDJY
Iodoacetic Acid
WF5188V710
Norepinephrine
X4W3ENH1CV
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
96-104Subventions
Organisme : Wellcome Trust
ID : 102645
Pays : United Kingdom
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