Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||The "Toll" of Opiod-Induced Glial Activation: Improving the Clinical Efficacy of Opioids by Targeting Glia|
|Citation:||Trends in Pharmacological Sciences, 2009; 30(11):581-591|
|Publisher:||Elsevier Science London|
|Linda R. Watkins, Mark R. Hutchinson, Kenner C. Rice, Steven F. Maier|
|Abstract:||Glial activation participates in the mediation of pain including neuropathic pain, due to release of neuroexcitatory, proinflammatory products. Glial activation is now known to occur in response to opioids as well. Opioid-induced glial activation opposes opioid analgesia and enhances opioid tolerance, dependence, reward and respiratory depression. Such effects can occur, not via classical opioid receptors, but rather via non-stereoselective activation of toll-like receptor 4 (TLR4), a recently recognized key glial receptor participating in neuropathic pain as well. This discovery identifies a means for separating the beneficial actions of opioids (opioid receptor mediated) from the unwanted side-effects (TLR4/glial mediated) by pharmacologically targeting TLR4. Such a drug should be a stand-alone therapeutic for treating neuropathic pain as well. Excitingly, with newly-established clinical trials of two glial modulators for treating neuropathic pain and improving the utility of opioids, translation from rats-to-humans now begins with the promise of improved clinical pain control.|
Drug Delivery Systems
Toll-Like Receptor 4
Clinical Trials as Topic
|Description:||Copyright © 2009 Elsevier Ltd All rights reserved.|
|Appears in Collections:||Aurora harvest 5|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.