Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination

Benjamin Gelman, N. Rifai, J. F. Goodrum, T. W. Bouldin, M. R. Krigman

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Apolipoprotein E (apo E) is synthesized and released in greatly increased amounts by peripheral nerve following Wallerian degeneration; it has been suggested that this protein may function in the transport of degenerated myelin lipid. The purpose of this study was to determine if the amount of apo E released by rat peripheral nerve is increased following selective demyelination, in the absence of significant axonopathy. Using an immunoturbidimetric assay, release of apo E from excised sciatic nerve segments was measured during the phases of acute demyelination and remyelination caused by tellurium (Te) toxicity, during segmental demyelination in chronic lead (Pb) poisoning, and during Wallerian degeneration following nerve crush. Morphologic changes were examined in contralateral sciatic nerves by nerve-fiber teasing or by light and electron microscopy of transverse sections. As in previous studies, the amount of apo E released from the nerves was greatly increased following Wallerian degeneration due to nerve crush. In Te neuropathy, increased release of apo E was first detected on the fourth day of Te exposure, corresponding temporally to the acute onset of paralysis and segmental demyelination. Apolipoprotein E release rose steeply to a maximum of ten times the control values by day 9 and then gradually waned during the next five weeks, corresponding to a period of active remyelination and resolution of the neuropathy. In the demyelinating neuropathy of chronic lead poisoning, apo E release was increased four times over control animals after seven weeks of exposure, with less than 10% of teased fibers showing early paranodal demyelination and no evidence of remyelination. Thus, apo E release by rat peripheral nerve stimulated during the acute phase of segmental demyelination, during active remyelination, and during Wallerian degeneration. The fact that the release of apo E is increased in the absence of significant axonal degeneration suggests that the increase observed during Wallerian degeneration is associated in part with the degeneration of the myelin sheath.

Original languageEnglish (US)
Pages (from-to)644-652
Number of pages9
JournalJournal of Neuropathology and Experimental Neurology
Volume46
Issue number6
StatePublished - 1987
Externally publishedYes

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Demyelinating Diseases
Apolipoproteins E
Sciatic Nerve
Wallerian Degeneration
Tellurium
Peripheral Nerves
Nerve Crush
Lead Poisoning
Myelin Sheath
Nerve Fibers
Paralysis
Electron Microscopy
Lipids
Light

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuroscience(all)

Cite this

Gelman, B., Rifai, N., Goodrum, J. F., Bouldin, T. W., & Krigman, M. R. (1987). Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination. Journal of Neuropathology and Experimental Neurology, 46(6), 644-652.

Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination. / Gelman, Benjamin; Rifai, N.; Goodrum, J. F.; Bouldin, T. W.; Krigman, M. R.

In: Journal of Neuropathology and Experimental Neurology, Vol. 46, No. 6, 1987, p. 644-652.

Research output: Contribution to journalArticle

Gelman, B, Rifai, N, Goodrum, JF, Bouldin, TW & Krigman, MR 1987, 'Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination', Journal of Neuropathology and Experimental Neurology, vol. 46, no. 6, pp. 644-652.
Gelman, Benjamin ; Rifai, N. ; Goodrum, J. F. ; Bouldin, T. W. ; Krigman, M. R. / Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination. In: Journal of Neuropathology and Experimental Neurology. 1987 ; Vol. 46, No. 6. pp. 644-652.
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