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Summary Experiments were performed to block molecules with antibodies which are 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 hemidenervated 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 a-bungarotoxin and of axons with 4D1-2ASP. Normally, endplates were completely reinnervated by 13–14 days (108 endplates in seven muscles). After daily application of polyclonal antibodies against NCAM or tenascin, reinnervation was significantly delayed. Preimmune serum, rabbit immunoglobulins or saline did not show this effect. Several monoclonal antibodies against NCAM (H-28) and tenascin (576, 578, 630, 633) showed a tendency but no significant effect. It is concluded that both NCAM and tenascin, upregulated after denervation, are involved in axon guidance and/or endplate reinnervation.

Summary Repeatedin vivo observations of vitally stained neuromuscular junctions allow direct monitoring of ongoing structural changes, although, normally occurring changes (remodelling) and those inflicted by the illumination itself (photodamage) need to be dissociated. In frog cutaneus pectoris muscles, stainedin vivo with 4Di-2ASP twice within four to five weeks, growth only was observed in 14 out of 92 junctions (in 18 muscles), retraction only in 19, and both features simultaneously in 22 junctions, while 37 junctions showed no changes. The summed growth in a junction amounted to 5–42 µm, retraction to 5–52 µm, while overall changes in synaptic length were absent. This and the simultaneous occurrence of both, growth and retraction within a single junction, indicates junctional remodelling. Similar amounts of remodelling were observed in junctions illuminated for 180, 60 or 10–30 s, indicating that within this range and with the given optical system, blue light and 4Di-2ASP fluorescence were not harmful. Remodelling was not induced by the experimental procedure per se, since inin vitro preparations signs of sprouting (and retraction) were equally frequent in junctions of totally untreated muscles, in junctions vitally stained four to five weeks previously or vitally stained but not light-exposed in the same muscle.