Polyclonal antibodies against NCAM reduce paralysis-induced axonal sprouting.
The neural cell adhesion molecule (NCAM) is upregulated in paralyzed muscles but the functional role of this upregulation is not clear. We have investigated the possible involvement of NCAM in botulinum toxin-induced axonal sprouting in mouse soleus muscles. Starting 4 days after botulinum toxin-A injection, the paralyzed muscles were exposed daily for 6 or 10 days to either rabbit polyclonal NCAM antibody or control solutions (preimmune serum or saline) or remained without further treatment. By 10 days after botulinum toxin injection, the mean number of sprouts and the mean total length of sprouts, respectively, in zinc iodide-osmium-stained preparations were 2.2 and 212 microm in untreated and control treated muscles but 1.0 and 51 microm in anti-NCAM treated muscles. By 14 days, the mean number of sprouts rose to 2.9 in untreated muscles but only 1.6 in anti-NCAM treated muscles. Macrophages/monocytes, probably originating from neighboring tissue damaged by the daily injections, were present in muscles of all groups. No T lymphocytes and no signs of muscle fiber damage were found, however, rendering antibody-mediated cytotoxic reactions as unlikely. From the blocking effects of anti-NCAM, it is concluded that NCAM plays a major role in the growth of paralysis-induced axonal sprouts.[1]References
- Polyclonal antibodies against NCAM reduce paralysis-induced axonal sprouting. Schäfer, R., Wernig, A. J. Neurocytol. (1998) [Pubmed]
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