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A new concept affecting restoration of inflammation-reactive astrocytes.

Journal article
Authors Linda Block
Ulrika Björklund
Anna Westerlund
P Jörneberg
Björn Biber
Elisabeth Hansson
Published in Neuroscience
Volume 250
Pages 536-45
ISSN 1873-7544
Publication year 2013
Published at Institute of Clinical Sciences, Department of Anesthesiology and Intensive care
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Pages 536-45
Language en
Subject categories Anesthesiology and Intensive Care


Long-lasting pain may partly be a consequence of ongoing neuroinflammation, in which astrocytes play a significant role. Following noxious stimuli, increased inflammatory receptor activity, influences in Na(+)/K(+)-ATPase activity and actin filament organization occur within the central nervous system. In astrocytes, the Ca(2+) signaling system, Na(+) transporters, cytoskeleton, and release of pro-inflammatory cytokines change during inflammation. The aim of this study was to restore these cell parameters in inflammation-reactive astrocytes. We found that the combination of (1) endomorphin-1, an opioid agonist that stimulates the Gi/o protein of the μ-opioid receptor; (2) naloxone, an opioid antagonist that inhibits the Gs protein of the μ-opioid receptor at ultralow concentrations; and (3) levetiracetam, an anti-epileptic agent that counteracts the release of IL-1β, managed to activate the Gi/o protein and Na(+)/K(+)-ATPase activity, inhibit the Gs protein, and decrease the release of IL-1β. The cell functions of astrocytes in an inflammatory state were virtually restored to their normal non-inflammatory state and it could be of clinical significance and may be useful for the treatment of long-term pain.

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