• M Devor, W Jänig, and M Michaelis.
• Department of Cell and Animal Biology, Hebrew University of Jerusalem, Israel.
• J. Neurophysiol. 1994 Jan 1;71(1):38-47.

Abstract1. Teased-fiber recordings were made from the axons of dorsal root ganglion (DRG) neurons in rats that underwent transection of the sciatic nerve 4-22 days previously. Many of the neurons had spontaneous ectopic discharge originating from within the DRG. 2. When postganglionic sympathetic efferents ending in the DRG were activated by tetanic stimulation of the T13 and L1 ventral roots (VRs), the ongoing afferent discharge was altered in more than one-half of the DRG neurons sampled. In most of the responsive units (62%), activity was augmented by this sympathetic stimulation; in the remainder (38%), activity was suppressed. Single-pulse stimuli of sympathetic efferents had no effect. 3. Responses to sympathetic stimulation began after a substantial delay (mean 14.3 s), peaked after 10-20 s, and then returned toward baseline over an additional 20-30 s. 4. Both excitatory and suppressive responses to sympathetic stimulation, as well as corresponding responses to systemically applied adrenaline, were blocked by the alpha-adrenoreceptor antagonist phentolamine. 5. Most of the active DRG neurons that responded to sympathetic stimulation, as well as others that did not, were excited by tetanic stimulation of neighboring afferent neurons that share the same DRG. These "crossed afterdischarge" responses were not blocked by phentolamine. Single-pulse stimuli of neighboring afferents had no effect. 6. Sympathetic-sensory coupling in DRGs of nerve-injured animals provides a previously unsuspected substrate for sympathetic involvement in neuropathic sensory dysfunction.

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