Functional μ opioid receptors are reduced in the spinal cord dorsal horn of diabetic rats

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Abstract

Background: The mechanisms of decreased spinal analgesic potency of morphine in neuropathic pain are not fully known. Agonist-stimulated [35S]GTPγS receptor autoradiography has been used to measure receptor activation of G proteins in vitro. Using this technique, we determined changes in the functional μ opioid receptors in the spinal dorsal horn in diabetic rats. Methods: Rats were rendered diabetic with an intraperitoneal injection of streptozotocin. The lumbar spinal cord was obtained from age-matched normal and diabetic rats 4 weeks after streptozotocin treatment. [D-Ala2,N-MePhe4,Gly5-ol]-enkephalin (DAMGO, 10 μM)-stimulated [35S]GTPγS binding was performed in both tissue sections and isolated membranes. Results: The DAMGO-stimulated [35S]GTPγS binding in the spinal dorsal horn was significantly reduced (approximately 37%) in diabetic rats compared with normal rats. However, [35S]GTPγS bindings in the spinal dorsal horn stimulated by other G protein-coupled receptor agonists, including [D-Pen2,D-Pen5]-enkephalln, R(-)N6-(2-phenylisopropyl)-adenosine, and WIN-55212, were not significantly altered in diabetic rats. The basal [35S]GTPγS binding in the spinal dorsal horn was slightly (approximately 13%) but significantly increased in diabetic rats. Western blot analysis revealed no significant difference in the expression of the α subunits of Gi and Go proteins in the dorsal spinal cord between normal and diabetic rats. Conclusions: These data suggest that the functional μ opioid receptors in the spinal cord dorsal horn of diabetic rats are reduced. The impaired functional μ opioid receptors in the spinal cord may constitute one of the mechanisms underlying the reduced spinal analgesic effect of μ opioids in diabetic neuropathic pain.

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Chen, S. R., Sweigart, K. L., Lakoski, J. M., & Pan, H. L. (2002). Functional μ opioid receptors are reduced in the spinal cord dorsal horn of diabetic rats. Anesthesiology, 97(6), 1602–1608. https://doi.org/10.1097/00000542-200212000-00037

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