Tissue plasminogen activator contributes to morphine tolerance and induces mechanical allodynia via astrocytic IL-1β and ERK signaling in the spinal cord of mice

Graphical abstract Chronic morphine treatment induces up-regulation of tissue plasminogen activator (tPA) in spinal cord astrocytes. tPA causes activation of ERK and increased synthesis of IL-1β, leading to antinociceptive tolerance. Spinal injection of tPA also induces astrogliosis and pain hyperse...

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Veröffentlicht in:	Neuroscience 2013-09, Vol.247, p.376-385
Hauptverfasser:	Berta, T, Liu, Y.-C, Xu, Z.-Z, Ji, R.-R
Format:	Artikel
Sprache:	eng
Schlagworte:	acute opioid analgesia Analgesics Animals Astrocytes - metabolism Biological and medical sciences chronic morphine exposure Drug Tolerance - physiology extracellular signal-regulated kinase (ERK) Fundamental and applied biological sciences. Psychology Hyperalgesia - metabolism Hyperalgesia - pathology Injections, Spinal interleukin-1 beta (IL-1β) Interleukin-1beta - biosynthesis Male MAP Kinase Signaling System - physiology Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Morphine - administration & dosage Neurology Neuropharmacology Pharmacology. Drug treatments Phosphorylation protease Signal Transduction - physiology Spinal Cord - metabolism Tissue Plasminogen Activator - deficiency tPA knockout mice Vertebrates: nervous system and sense organs
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Zusammenfassung:	Graphical abstract Chronic morphine treatment induces up-regulation of tissue plasminogen activator (tPA) in spinal cord astrocytes. tPA causes activation of ERK and increased synthesis of IL-1β, leading to antinociceptive tolerance. Spinal injection of tPA also induces astrogliosis and pain hypersensitivity.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2013.05.018