Ectopic adrenergic sensitivity in damaged peripheral nerve axons in the rat

Ernesto M.D. Korenman, Marshall Devor*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

124 Scopus citations

Abstract

Single-fiber recordings were made of impulses generated ectopically in nerve end neuromas. Most spontaneously active sensory fibers and some otherwise silent sensory fibers responded to adrenergic agonists injected close arterially or into the general circulation by way of the jugular vein. There was α-adrenergic pharmacology. Motor fibers were insensitive. To obtain equivalent neural responses, an intravenous dose about 10 times the close arterial dose was required. Many neuroma fibers responded to local ischemia. The response to adrenalin, however, could still be demonstrated in ischemic neuromas. The effect of adrenergic stimulation is therefore not due solely to a local change of blood flow. Tetanic stimulation of the preganglionic sympathetic column altered neuroma discharge in both intact and adrenalectomized rats in the same way that systemic adrenalin did. The results support the hypothesis that damaged sensory axons develop ectopic α-adrenergic receptors that render them sensitive to sympathetic activity. This might explain the success of surgical and chemical sympathectomy in alleviating pain in some cases of peripheral nerve injury.

Original languageEnglish
Pages (from-to)63-81
Number of pages19
JournalExperimental Neurology
Volume72
Issue number1
DOIs
StatePublished - Apr 1981

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