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The Journal of Neuroscience, January 23, 2008, 28(4):904-913; doi:10.1523/JNEUROSCI.4452-07.2008

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Behavioral/Systems/Cognitive
Spinal µ-Opioid Receptor-Expressing Dorsal Horn Neurons: Role in Nociception and Morphine Antinociception

Robert H. Kline, IV^1,3 and Ronald G. Wiley^1,2,3,4

¹Laboratory of Experimental Neurology and ²Neurology Service Veterans Affairs, Tennessee Valley Healthcare System, Nashville, Tennessee 37212-2637, and Departments of ³Neurology and ⁴Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37212

Correspondence should be addressed to Dr. Ronald G. Wiley, Departments of Neurology and Pharmacology, Vanderbilt University School of Medicine, 1310 24th Avenue South, Nashville, TN 37212. Email: ronald.wiley{at}vanderbilt.edu

The role of spinal cord µ-opioid receptor (MOR)-expressing dorsal horn neurons in nociception and morphine analgesia is incompletely understood. Using intrathecal dermorphin-saporin (Derm-sap) to selectively destroy MOR-expressing dorsal horn neurons, we sought to determine the role of these neurons in (1) normal baseline reflex nocifensive responses to noxious thermal stimulation (hotplate, tail flick) and to persistent noxious chemical stimulation (formalin) and (2) the antinociceptive activity of intrathecal and systemic morphine in the same tests. Lumbar intrathecal Derm-sap (500 ng) produced (1) partial loss of lamina II MOR-expressing dorsal horn neurons, (2) no effect on MOR-expressing dorsal root ganglion neurons, and (3) no change in baseline tail-flick and hotplate reflex nocifensive responses. Derm-sap treatment attenuated the antinociceptive action of both intrathecal and systemic morphine on hotplate responses. Derm-sap treatment had two effects in the formalin test: (1) increased baseline nocifensive responding and (2) reduced antinociceptive action of systemic morphine. We conclude that MOR-expressing dorsal horn neurons (1) are not essential for determining nocifensive reflex responsiveness to noxious thermal stimuli, (2) are necessary for full antinociceptive action of morphine (intrathecal or systemic) in these tests, and (3) play a significant role in the endogenous modulation of reflex nocifensive responses to persistent pain in the formalin test. Thus, one would predict that altering the activity of MOR-expressing dorsal horn neurons would be antinociceptive and of interest in the search for new approaches to management of chronic pain.

Key words: dermorphin; saporin; µ-opioid receptor; intrathecal morphine; pain; reflex modulation; molecular neurosurgery

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Received Sept. 28, 2007; revised Dec. 11, 2007; accepted Dec. 11, 2007.

Correspondence should be addressed to Dr. Ronald G. Wiley, Departments of Neurology and Pharmacology, Vanderbilt University School of Medicine, 1310 24th Avenue South, Nashville, TN 37212. Email: ronald.wiley{at}vanderbilt.edu

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