Modulation of Spinal-cord Function by Anesthesia

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Abstract
Two forms of presynaptic depolarization occur in experimental animals, and probably in man. The 1st form, reflected in the 1st component of the dorsal cord potential, is independent of the existence or the state of activity of supraspinal structures, is enhanced by thiamylal, and is suppressed by ketamine and bicuculline. It is probably mediated by .gamma.-aminobutyric acid. The 2nd form, reflected in the 2nd component of the dorsal cord potential, probably requires increased stimulus intensity for its production, is dependent upon supraspinal structures, is suppressed by thiamylal, and is facilitated or unaffected by bicuculline or by ketamine. Different loci are suggested on the dorsal root fibers for the 2 effects, different pathways, both spinal and supraspinal, and/or different transmitters. In single-unit studies is spinal cats, ketamine suppressed single units in those dorsal horn laminae concerned with the processing of information related to noxious stimuli. Barbiturates, have a tendency to suppress all dorsal horn laminae tested.