title: Spinal recordings suggest that wide-dynamic-range neurons mediate sympathetically maintained pain.
abstract: In order to determine which classes of spinal neurons are capable of mediating sympathetically maintained pain, recordings were made from single somatosensory neurons in spinal cords of anesthetized cats. Each neuron was functionally identified with mechanical stimuli, and its responses to electrical stimulation of the sympathetic trunk were recorded. Nearly half (45%) of the wide-dynamic-range (WDR) neurons tested were activated by sympathetic stimulation, but none of the high threshold (nociceptor-specific) neurons and only 17% of the low threshold neurons were activated. Sympathetic activation was most common for WDR neurons that had the following: receptive fields proximal to the toes, low thresholds for mechanical activation, and both rapidly and slowly adapting responses to pressure. The predominant WDR response to sympathetic stimulation was long latency (greater than 1 sec) excitation. Sympathetic activation of WDR neurons was abolished by each of the following procedures: subcutaneous injection of local anesthetic, cooling of the receptive field with ice, and intravenous injection of the alpha-adrenergic blocker, phentolamine. The axons of some sympathetically activated WDR were shown to project to higher centers. These results indicate that WDR neurons are the only spinal nociceptive neurons activated by sympathetic efferent activity in this preparation. Therefore, WDR neurons, rather than high threshold neurons, are most likely to mediate the spinal component of sympathetically maintained pain. These results provide supporting evidence for our previous hypothesis that sympathetically maintained pain is mediated by myelinated mechanoreceptors acting on sensitized WDR neurons. Our results also demonstrate that sympathetic activation of WDR neurons is mediated by an alpha-adrenergic mechanism in the skin.
authors.affiliation: Neurological Sciences Institute, Good Samaritan Hospital and Medical Center, Portland, OR 97209 U.S.A.
authors.forename: William J
authors.initials: WJ
authors.lastname: Roberts
authors.forename: Mark E
authors.initials: ME
authors.lastname: Foglesong
mesh_terms: D000222:Adaptation, Physiological; D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D005260:Female; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009475:Neurons, Afferent / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D010646:Phentolamine / Q000494:pharmacology; D010812:Physical Stimulation; D012684:Sensory Thresholds; D013116:Spinal Cord / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D008012:Lidocaine; D010646:Phentolamine