Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/43168
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dc.contributor.authorWatkins, L.en
dc.contributor.authorHutchinson, M.en
dc.contributor.authorJohnston, I.en
dc.contributor.authorMaier, S.en
dc.date.issued2005en
dc.identifier.citationTrends in Neurosciences, 2005; 28(12):661-669en
dc.identifier.issn0166-2236en
dc.identifier.issn1878-108Xen
dc.identifier.urihttp://hdl.handle.net/2440/43168-
dc.description.abstractDevelopment of analgesic tolerance and withdrawalinduced pain enhancement present serious difficulties for the use of opioids for pain control. Although neuronal mechanisms to account for these phenomena have been sought for many decades, their bases remain unresolved. Within the past four years, a novel nonneuronal candidate has been uncovered that opposes acute opioid analgesia and contributes to development of opioid tolerance and tolerance-associated pain enhancement. This novel candidate is spinal cord glia. Glia are important contributors to the creation of enhanced pain states via the release of neuroexcitatory substances. New data suggest that glia also release neuroexcitatory substances in response to morphine, thereby opposing its effects. Controlling glial activation could therefore increase the clinical utility of analgesic drugs.en
dc.language.isoenen
dc.publisherElsevier Science Londonen
dc.subjectBrain; Spinal Cord; Neuroglia; Nociceptors; Animals; Humans; Pain; Neurotransmitter Agents; Analgesics, Opioid; Drug Toleranceen
dc.titleGlia: novel counter-regulators of opioid analgesiaen
dc.typeJournal articleen
dc.identifier.rmid0020083019en
dc.identifier.doi10.1016/j.tins.2005.10.001en
dc.identifier.pubid41740-
pubs.library.collectionEarth and Environmental Sciences publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidHutchinson, M. [0000-0003-2154-5950]en
Appears in Collections:Earth and Environmental Sciences publications

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