Functional axonal regeneration can occur in the adult mammalian peripheral nervous System (PNS) after nerve damage wheras little spontaneous axonal regrowth occurs following lesions in the mature central nervous System (CNS). At the molecular level one of the most prominent effects following injury of mature peripheral and central nerves is the Stimulation of synthesis and secretion of a 37 k protein (1,2) which accu-mulates only in regenerating peripheral nerve (3). The lesion-induced 37 k protein in rat PNS has recently been identified as a form of apolipoprotein E (apoE) (4). Here we describe the immunocytochemical identification of the cell types expressing the 37 k protein/apoE in developing, mature and injured rat PNS and CNS. In the mature PNS 37 k protein/apoE like immunoreactivity was associated with the basal lamina, whereas after injury the immunoreactivity appeared in infiltrating (hematogenous) macrophages. In the CNS, 37 k protein/apoE-like immunoreactivity was clearly associated with the cell bodies and processes of astrocytes. These cells rapidly lost their immunoreactivity after injury. The specific differences between macrophages and astrocytes in their response to injury of peripheral and central nerves respectively, may account for or relate to the known limitations of the ability of injured CNS neurons to regenerate. In contrast, the specific expression of the 37 k protein/apoE by macrophages in the PNS and astrocytes in the CNS newborn rats indicates a previously unexpected common function of these ontogenetically unrelated cell types in nerve development and/or maturation.


  1. 1.
    Skene JHP, Shooter EM (1983) Proc Natl Acad Sci USA 80:4169PubMedCrossRefGoogle Scholar
  2. 2.
    Müller HW, et al. (1986) J Cell Biol 102:393PubMedCrossRefGoogle Scholar
  3. 3.
    Müller HW, et al. (1985) Science 228:499PubMedCrossRefGoogle Scholar
  4. 4.
    Ignatius MJ, et al. (1987) Proc Natl Acad Sci USA (in press)Google Scholar

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© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • G. Stoll
  • H. W. Müller

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