Glial cell responses, complement and apolipoprotein J expression following axon injury in the neonatal rat.
Immature motoneurons are highly susceptible to degeneration following axon injury. The response of perineuronal glia to axon injury may significantly influence neuronal survival and axon regeneration. We have examined the central reactions to neonatal facial nerve transection with emphasis on the expression of complement component C3 (C3) and the multifunctional apolipoprotein J (ApoJ). Axotomy was performed on one-day-old rats. Animals were perfused from eight hours to two weeks after the lesion. The astroglial marker, glial fibrillary acidic protein (GFAP) was increased from one day and the microglial marker OX-42 from two days after injury. ApoJ immunoreactivity was increased in axotomized neuronal perikarya and astroglial cells from one day postaxotomy, but no C3 immunoreactive profiles were found at any postoperative survival time. Cell proliferation as judged by bromodeoxyuridine labeling and immunoreactivity for the cyclin Ki-67 antigen (antibody MIB5) occurred only at two days after injury. Double immunostaining revealed that the vast majority of proliferating cells were microglia, although occasional cells double labeled astrocytes were found as well. Our results indicate that the non-neuronal response in neonatal animals differ from that of adult ones as follows: 1) microglia transform rapidly into phagocytes in parallel with the degeneration of axotomized neurons, 2) despite the presence of neuronal degeneration, no expression of C3 was found, and the upregulation of the expression of the complement C3 receptor (CR3) is delayed, 3) ApoJ is strongly upregulated in perineuronal astrocytes as well as in the axotomized motoneurons. The marked upregulation of ApoJ in both instances suggests a general role of this protein in the neuronal response to axotomy.
Tao
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R
Department of Neuroscience, Division of Neuroanatomy, Biomedical Center, P.O. Box 587, SE-751 23 Uppsala, Sweden.
Aldskogius
H
H
D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000166:cytology / Q000502:physiology; D019771:Axotomy; D002455:Cell Division; D051152:Clusterin; D003176:Complement C3 / Q000032:analysis / Q000096:biosynthesis*; D005154:Facial Nerve / Q000502:physiology*; D019084:Fluorescent Antibody Technique, Indirect; D005786:Gene Expression Regulation; D006023:Glycoproteins / Q000032:analysis / Q000096:biosynthesis*; D007150:Immunohistochemistry; D017628:Microglia / Q000166:cytology / Q000502:physiology; D018832:Molecular Chaperones; D009410:Nerve Degeneration / Q000503:physiopathology*; D009416:Nerve Regeneration / Q000502:physiology*; D009457:Neuroglia / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D009836:Oligodendroglia / Q000166:cytology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley
D051152:Clusterin; D003176:Complement C3; D006023:Glycoproteins; D018832:Molecular Chaperones