Transsynaptic degeneration in the superficial dorsal horn after sciatic nerve injury: effects of a chronic constriction injury, transection, and strychnine

Tomosada Sugimoto, Gary J. Bennett, Keith C. Kajander

Research output: Contribution to journalArticle

298 Citations (Scopus)

Abstract

The lumbar and cervical spinal dorsal horns of adult rats with a chronic (8 days) constriction injury of the sciatic nerve on one side (and a sham operation on the other) were examined for signs of transsynaptic degeneration. The incidence of neurons with signs of degeneration (pyknosis and hyperchromatosis; 'dark neurons') was significantly increased in the lumbar dorsal horn on both sides. The ipsilateral lumbar increase was significantly greater than the contralateral increase. There was no increase in the incidence of dark neurons in the cervical dorsal horns of the same rats. The distribution of lumbar dark neurons was similar bilaterally. The majority of the dark neurons were found in the sciatic nerve's territory in laminae I-II. A second group of rats received the same surgery but in addition received a series of 7 daily subconvulsive doses of strychnine. Dark neurons were again found bilaterally (with ipsilateral predominance) in the sciatic nerve's territory in lumbar laminae I-II, but the incidence was significantly greater than that found in the group that did not receive strychnine. The same result was obtained in a third group of strychnine-treated rats when the sham operation was omitted. Thus the appearance of contralateral dark neurons is not dependent on unintentional nerve damage created by the sham procedure. An additional group of rats was sacrificed 8 days after receiving a unilateral sciatic nerve transection, a contralateral sham operation, and the 7 daily strychnine injections. There was no increase in the incidence of dark neurons in any of these rats. The chronic constriction injury produces signs of neuropathic pain, including hyperalgesia, allodynia, and spontaneous pain (or dysesthesia). The finding that the constriction injury evokes transsynaptic degeneration in spinal dorsal horn neurons suggests that a central anatomical abnormality might be responsible for one or more of the abnormalities of pain sensation.

Original languageEnglish
Pages (from-to)205-213
Number of pages9
JournalPain
Volume42
Issue number2
DOIs
Publication statusPublished - Aug 1990

Keywords

  • Causalgia
  • Neuropathic pain
  • Peripheral neuropathy
  • Reflex sympathetic dystrophy
  • Transsynaptic degeneration

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Anesthesiology and Pain Medicine

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