POLYCLONAL ANTIBODIES AGAINST NCAM AND TENASCIN DELAY END-PLATE REINNERVATION

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.