Experimental peripheral neuropathy decreases the dose of substance P required to increase excitatory amino acid release in the CSF of the rat spinal cord

Stephen R. Skilling, Donald H. Harkness, Alice A. Larson

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

Partial ligation of the sciatic nerve of rats produces hyperalgesia similar to that seen in humans following nerve injury. In this study, we used microdialysis of the spinal cord cerebral spinal fluid (CSF) to test the hypothesis that hyperalgesia is due to an enhanced release of excitatory amino acids (EAA) in response to substance P (SP). Intrathecal SP caused release of aspartate and glutamate in the CSF of rats with partial sciatic ligation at a dose of SP that did not cause release in sham operated animals. Neonatal capsaicin pretreatment blocked SP-induced EAA release in both sham and sciatic ligated animals. Release of EAAs in ligated animals was not significantly different from release in sham-operated animals following higher doses of SP or chemical nociceptive stimulation. These results demonstrate a partial sciatic ligation-induced decrease in the dose of SP required to initiate EAA release in the CSF of the spinal cord, a change which could play an important role in hyperalgesia.

Original languageEnglish (US)
Pages (from-to)92-96
Number of pages5
JournalNeuroscience Letters
Volume139
Issue number1
DOIs
StatePublished - May 11 1992

Bibliographical note

Funding Information:
This research was supported by United States Public Health Service Grants (DA04090, DA04190, DA00124) to A.A.L. and (CA01342) to S.R.S.

Keywords

  • Aspartate
  • Capsaicin, Mustard oil
  • Glutamate
  • Hyperalgesia
  • Pain
  • Primary afferent fiber

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