Central glucocorticoid receptors modulate the expression of spinal cannabinoid receptors induced by chronic morphine exposure

Central glucocorticoid receptors modulate the expression of spinal cannabinoid receptors induced... Central cannabinoid receptors (CBRs) have been implicated in the opioid analgesic effects. However, it remains unclear as to whether the expression of central CBRs would be altered after repeated morphine exposure. Here, we show that chronic intrathecal treatment with morphine (10 μg, twice daily for 6 days) induced a time-dependent upregulation of both CB-1 and CB-2 receptors within the spinal cord dorsal horn. This morphine-induced CB-1 and CB-2 upregulation was dose-dependently attenuated by the intrathecal co-administration of morphine with the glucocorticoid receptor (GR) antagonist RU38486 (0.25, 0.5, or 2 μg). The intrathecal RU38486 treatment regimen also attenuated the development of morphine tolerance. These results indicate that the expression of spinal CBRs was altered following repeated morphine exposure and regulated by the activation of central GRs. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Central glucocorticoid receptors modulate the expression of spinal cannabinoid receptors induced by chronic morphine exposure

Brain Research, Volume 1059 (1) – Oct 12, 2005

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Publisher
Elsevier
Copyright
Copyright © 2005 Elsevier B.V.
ISSN
0006-8993
D.O.I.
10.1016/j.brainres.2005.08.002
Publisher site
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Abstract

Central cannabinoid receptors (CBRs) have been implicated in the opioid analgesic effects. However, it remains unclear as to whether the expression of central CBRs would be altered after repeated morphine exposure. Here, we show that chronic intrathecal treatment with morphine (10 μg, twice daily for 6 days) induced a time-dependent upregulation of both CB-1 and CB-2 receptors within the spinal cord dorsal horn. This morphine-induced CB-1 and CB-2 upregulation was dose-dependently attenuated by the intrathecal co-administration of morphine with the glucocorticoid receptor (GR) antagonist RU38486 (0.25, 0.5, or 2 μg). The intrathecal RU38486 treatment regimen also attenuated the development of morphine tolerance. These results indicate that the expression of spinal CBRs was altered following repeated morphine exposure and regulated by the activation of central GRs.

Journal

Brain ResearchElsevier

Published: Oct 12, 2005

References

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