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In behavioral tests, rats performed learned escape responses to thermal stimulation of the paws by 44.0. 47.0. or 0.3 degrees C. Licking, guarding, and jumping reflexes were evaluated at these temperatures. The frequency, latency, and duration of escape and reflex responses were compared and were related to hind-paw skin temperatures measured during stimulation of awake and anesthetized rats. The duration and latency of escape from heat were appropriately related to stimulus intensity. Escape occurred reliably for each intensity. Reflexes occurred unreliably and at long latency to 44.0 or 0.3 degrees C and were not appropriately related to heat intensity. The reflexes were relatively insensitive to thermal nociceptive stimulation other than heating of the skin at a high rate.

The role of spinal cord -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.