title: Axon growth failure following corpus callosum lesions precedes glial reaction in perinatal rats.
abstract: The present study compares the glial reactivity and the axon growth following corpus callosum (CC) lesions, in perinatal rats. Lesions were performed on fetal (E17 to E20) and early postnatal (P0 and P2) rats. The reactive glia and the presence of neural fibers were detected by immunohistochemical staining of glial fibrillary acidic protein (GFAP) and neurofilament protein (NFP), respectively. The callosal axons failed (at least in part) to penetrate the lesioned area already after E18 lesions, and the lesioned area was always impenetrable for axons after E20 and P0 lesions. In these cases, the lesioned part of the CC was completely or nearly devoid of GFAP as well as NFP. The distributions of the immunopositivities to GFAP and NFP also coincided with each other, both in the intact part of the CC and along the alternative courses of the callosal axons. GFAP-immunopositive reactive glia accompanied to the deficiency of NFP-immunostaining only when animals were lesioned at P2. Nestin immunostaining revealed astrocytes or their precursors already at P0, but reactive glia were detected only after P2 lesions, as with immunostaining to GFAP. The results suggest that the age after which the lesioned area proves to be impenetrable for axons can precede that age after which lesions provoke glial reaction. In this case the inhibition of axon growth is to be attributed to factors other than to the reactive glia. The presence of nestin-positive cells suggests that the lack of reactive glia along the lesion track was not due to the absence of astrocytes, but rather due to the lack of their reaction to lesion. In this developmental stage astroglia, when activated, seem to promote the growth of axons.
authors.affiliation: Department of Anatomy, Histology and Embryology, Semmelweis University, Tüzoltó 58, Budapest, 1450 Hungary.
authors.forename: B M
authors.initials: BM
authors.lastname: Ajtai
authors.forename: M
authors.initials: M
authors.lastname: Kálmán
mesh_terms: D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001369:Axons / Q000378:metabolism / Q000473:pathology*; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology*; D003337:Corpus Callosum / Q000293:injuries* / Q000378:metabolism / Q000473:pathology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000196:embryology / Q000378:metabolism / Q000473:pathology*; D007150:Immunohistochemistry; D007381:Intermediate Filament Proteins / Q000378:metabolism; D008297:Male; D009412:Nerve Fibers / Q000378:metabolism / Q000473:pathology; D009416:Nerve Regeneration; D009419:Nerve Tissue Proteins; D064231:Nestin; D016900:Neurofilament Proteins / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D051381:Rats
chemical_list: D005904:Glial Fibrillary Acidic Protein; D007381:Intermediate Filament Proteins; D009419:Nerve Tissue Proteins; C577486:Nes protein, rat; D064231:Nestin; D016900:Neurofilament Proteins