Opioids and central sensitisation: II. Induction and reversal of hyperalgesia
- 1 April 2005
- journal article
- review article
- Published by Wiley in European journal of pain
- Vol. 9 (2) , 149-152
- https://doi.org/10.1016/j.ejpain.2004.05.011
Abstract
Opioids are powerful analgesics when used to treat acute pain and some forms of chronic pain. In addition, opioids can preempt some forms of central sensitization. Here we review evidence that opioids may also induce and perhaps reverse some forms of central sensitization.Keywords
This publication has 43 references indexed in Scilit:
- Short-term infusion of the μ-opioid agonist remifentanil in humans causes hyperalgesia during withdrawalPAIN®, 2003
- Morphine hyperalgesia: A case reportAmerican Journal of Hospice and Palliative Medicine®, 2003
- Long-term depression of excitatory synaptic transmission and its relationship to long-term potentiationPublished by Elsevier ,2003
- Differential Effects of μ-Opioid Receptor Ligands on Ca2+ SignalingThe Journal of Pharmacology and Experimental Therapeutics, 2002
- Reduced development of tolerance to the analgesic effects of morphine and clonidine in PKCγ mutant micePain, 2001
- Mechanisms of opioid-induced pain and antinociceptive tolerance: descending facilitation and spinal dynorphinPain, 2001
- Small-Dose Ketamine Enhances Morphine-Induced Analgesia After Outpatient SurgeryAnesthesia & Analgesia, 1999
- Chronic opioid treatment of neuroblastoma X dorsal root ganglion neuron hybrid F11 cells results in elevated GM1 ganglioside and cyclic adenosine monophosphate levels and onset of naloxone‐evoked decreases in membrane K+ currentsJournal of Neuroscience Research, 1995
- Protein kinase C reduces Mg2+ block of NMDA-receptor channels as a mechanism of modulationNature, 1992
- Sustained potentiation of NMDA receptor-mediated glutamate responses through activation of protein kinase C by a μ opioidNeuron, 1991