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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.identifier.citationTrends in Neurosciences, 2005; 28(12):661-669en
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.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
pubs.library.collectionEarth and Environmental Sciences publicationsen
dc.identifier.orcidHutchinson, M. [0000-0003-2154-5950]en
Appears in Collections:Earth and Environmental Sciences publications

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