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Polyclonal antibodies against NCAM and tenascin delay endplate reinnervation
B Langenfeld-Oster1, A Faissner, A Irintchev
1Department of Physiology (Neurophysiology), University of Bonn, Germany.
Abstract:
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 alpha-bungarotoxin and of axons with 4Di-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.
Insights
Antibodies blocking Neural Cell Adhesion Molecule (NCAM) and tenascin significantly delayed nerve regeneration in mouse muscles. These molecules, upregulated after denervation, are crucial for axon guidance and endplate reinnervation.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Molecular Biology
Background:
- Nerve injury, or denervation, leads to molecular changes in muscle and nerve tissues.
- Understanding the molecules involved in nerve regeneration is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the role of upregulated molecules, specifically Neural Cell Adhesion Molecule (NCAM) and tenascin, in nerve regeneration after denervation.
- To determine if blocking these molecules with antibodies affects the rate of endplate reinnervation.
Main Methods:
- Hemidenervation of the gluteus maximus muscle in mice by nerve freezing.
- Evaluation of endplate reinnervation using vital staining of acetylcholine receptors and axons.
- Application of polyclonal antibodies against NCAM and tenascin, or control substances, to assess their impact on regeneration.
Main Results:
- Endplate reinnervation typically occurred within 13-14 days in control groups.
- Daily application of polyclonal antibodies against NCAM and tenascin significantly delayed endplate reinnervation.
- Monoclonal antibodies showed a trend but did not significantly inhibit reinnervation.
Conclusions:
- Neural Cell Adhesion Molecule (NCAM) and tenascin play a significant role in the process of axon guidance and endplate reinnervation following denervation.
- Targeting NCAM and tenascin could be a potential therapeutic approach to modulate nerve regeneration.