Changes in innervation of long bones after insertion of an implant : immunocytochemical study in goats with antibodies to calcitonin gene-related peptide and B-50/GAP-43

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The growth-associated protein B-50 (GAP-43) in dystrophic neurites extending into Alzheimer's plaques

The expression of the growth associated protein B-50 (GAP-43) is developmentally regulated and reinduced following neuronal injury. Using B-50 as marker for sprouting in single and double immunolabeling of neocortex of Alzheimer's disease (AD) we demonstrate that bulbous B-50 immunoreactive dystrophic neurites are found in β-amyloid/A4 positive plaques. Our results and those of others indicate that dystrophic neurites contain B-50 implicating this protein in the disease induced response

Changes in the distribution of the neuron-specific B-50, neurofilament protein and glial fibrillary acidic proteins following an unilateral mesencephalic lesion in the rat

Following a unilateral electrolytic lesion in the ventral rat mesencephalon, changes in the immunocytochemical distribution of the neuron-specific B-50, neurofilament (NF) protein and glial fibrillary acidic (GFAP) proteins were studied around the lesion after 0, 3, 10 and 28 days. At all recovery times, the controls displayed on immunostaining with anti-B-50 and anti-neurofilament antibodies, a characteristic pattern of synaptic and neuritic localization of these antigens, whereas anti-GFAP staining revealed a distribution typical for astrocytes. The lesion was characterized by a center of coagulated material that exhibited immunoreactivity to B-50 (BIR) and NF (NFIR), but never GFAP-immunoreactivity. From 3 days on, the center became surrounded by disintegrating cells which were unreactive to the antibodies. The antigen distribution changed temporally, predominantly at the lesion rim. By 10 and 28 days postlesion, additional BIR was observed as punctuate dots in fibers and membranes of neurons. Enhanced NFIR was detected in fibers and cell bodies. Many astrocytes were detected around the lesion rim, forming by 28 days postsurgery a barrier between the lesion cavity and the uninjured tissue. Our study shows that distribution changes in B-50, NF and GFAP around the lesion may indicate local degenerative and adaptative processes as a temporal response to brain trauma