Axon growth failure following corpus callosum lesions precedes glial reaction in perinatal rats

The present study compares the glial reactivity and the axon growth followi ng corpus callosum (CC) lesions, in perinatal rats. Lesions were performed on fetal (E17 to E20) and early postnatal (P0 and P2) rats. The reactive gl ia and the presence of neural fibers were detected by immunohistochemical s taining of glial fibrillary acidic protein (GFAP) and neurofilament protein (NFP), respectively. The callosal axons failed (at least in part) to penet rate the lesioned area already after E18 lesions, and the lesioned area was always impenetrable for axons after E20 and P0 lesions. In these cases, th e lesioned part of the CC was completely or nearly devoid of GFAP as well a s NFP. The distributions of the immunopositivities to GFAP and NFP also coi ncided with each other, both in the intact part of the CC and along the alt ernative courses of the callosal axons. GFAP-immunopositive reactive glia a ccompanied to the deficiency of NFP-immunostaining only when animals were l esioned at P2. Nestin immunostaining revealed astrocytes or their precursor s 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 t he lesioned area proves to be impenetrable for axone can precede that age a fter which lesions provoke glial reaction. In this case the inhibition of a xon 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 gl ia along the lesion track was not due to the absence of astrocytes, but rat her due to the lack of their reaction to lesion. In this developmental stag e astroglia, when activated, seem to promote the growth of axons.