Journal of neurophysiology
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It was recently shown that repeated heat stimulation, using brief contacts (<1 s) with a preheated thermode at sufficiently short interstimulus intervals (ISIs <5 s) and high temperatures (> or =51 degrees C), will elicit in humans a sensation of rapidly augmenting "second" (burning) pain with only a weak "first" (sharp) pain sensation. Most strikingly, at short intertrial intervals (ITIs >5 s) such summation will reset, or begin again at baseline. In the present experiments, the responses of nociceptive lamina I spinothalamic (STT) neurons in the lumbosacral dorsal horn of barbiturate-anesthetized cats were examined using this repeated brief contact heat paradigm. ⋯ The summation and the reset displayed by HPC cells were not related to skin temperature. Thus the results presented in this study, together with those in the preceding article, demonstrate a double dissociation indicating that NS and HPC lamina I STT cells can subserve the qualitatively distinct sensations of first (sharp) and second (burning) pain, respectively. These findings support the concept that the lamina I STT projection comprises several discrete sensory channels that are integrated in the forebrain to generate distinct sensations.
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Pain has long been thought to wax and wane in relative proportion to fluctuations in the intensity of noxious stimuli. Dynamic aspects of nociceptive processing, however, remain poorly characterized. Here we show that small decreases (+/-1-3 degrees C) in noxious stimulus temperatures (47-50 degrees C) evoked changes in perceived pain intensity that were as much as 271% greater than those of equal magnitude increases. ⋯ Together, these findings indicate that an analgesic mechanism is activated during noxious stimulus offset. This analgesic phenomenon may serve as a temporal contrast enhancement mechanism to amplify awareness of stimulus offset and to reinforce escape behaviors. Disruption of this mechanism may contribute importantly to chronic pain.
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Activation of spinal alpha(2)-adrenergic receptors by the descending noradrenergic system and alpha(2)-adrenergic agonists produces analgesia. However, the sites and mechanisms of the analgesic action of spinally administered alpha(2)-adrenergic receptor agonists such as clonidine are not fully known. The dorsal horn neurons in the outer zone of lamina II (lamina II(o)) are important for processing nociceptive information from C-fiber primary afferents. ⋯ The effect of clonidine on evoked EPSCs was abolished in the presence of yohimbine (n = 5). These data suggest that clonidine inhibits the excitatory synaptic input to lamina II(o) neurons through activation of alpha(2)-adrenergic receptors located on the glutamatergic afferent terminals. Presynaptic inhibition of glutamate release from primary afferents onto lamina II(o) neurons likely plays an important role in the analgesic action produced by activation of the descending noradrenergic system and alpha(2)-adrenergic agonists.