B. Langenfeldoster et al., POLYCLONAL ANTIBODIES AGAINST NCAM AND TENASCIN DELAY END-PLATE REINNERVATION, Journal of neurocytology, 23(10), 1994, pp. 591-604
Experiments were performed to block molecules with antibodies which ar
e upregulated in nerve and muscle following denervation. The delay in
endplate reinnervation was taken as a measure for their involvement in
regeneration. Gluteus maximus muscles of 86 male CBA/J mice were hemi
denervated by freezing the caudal gluteal nerve at a defined position.
The degree of reinnervation was evaluated in identified endplates by
repeated vital staining of ACh receptors with rhodaminated cu-bungarot
oxin and of axons with 4Di-2ASP. Normally, endplates were completely r
einnervated by 13-14 days (108 endplates in seven muscles). After dail
y application of polyclonal antibodies against NCAM or tenascin, reinn
ervation was significantly delayed. Preimmune serum, rabbit immunoglob
ulins or saline did not show this effect. Several monoclonal antibodie
s against NCAM (H-28) and tenascin (576, 578, 630, 633) showed a tende
ncy but no significant effect. It is concluded that both NCAM and tena
scin, upregulated after denervation, are involved in axon guidance and
/or endplate reinnervation.