The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle‐specific nicotinic acetylcholine receptor

• Published in: Developmental neurobiology (Hoboken, N.J.) Vol. 68; no. 7; pp. 972 - 980
• Main Authors: Oppenheim, Ronald W., Calderó, Jordi, Cuitat, Doloros, Esquerda, Josep, McArdle, Joseph J., Olivera, Baldomero M., Prevette, David, Teichert, Russell W.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-06-2008
• Subjects: acetylcholine receptor; Animals; Apoptosis - drug effects; Apoptosis - physiology; Axons - drug effects; Axons - physiology; Bungarotoxins - pharmacology; cell death; Cell Survival; Chick Embryo; Conotoxins - pharmacology; Curare - pharmacology; motoneurons; Motor Neurons - cytology; Motor Neurons - drug effects; Motor Neurons - physiology; Movement - drug effects; muscle; Neuromuscular Junction - cytology; Neuromuscular Junction - drug effects; Neuromuscular Junction - embryology; Nicotinic Antagonists - pharmacology; Peptides, Cyclic - pharmacology; Receptors, Nicotinic - physiology; Tubulin - metabolism
• ISSN: 1932-8451; 1932-846X
• DOI: 10.1002/dneu.20636

In an attempt to determine whether the rescue of developing motoneurons (MNS) from programmed cell death (PCD) in the chick embryo following reductions in neuromuscular function involves muscle or neuronal nicotinic acetylcholine receptors (nAChRs), we have employed a novel cone snail toxin αA‐OIVA that acts selectively to antagonize the embryonic/fetal form of muscle nAChRs. The results demonstrate that αA‐OIVA is nearly as effective as curare or α‐bungarotoxin (α‐BTX) in reducing neuromuscular function and is equally effective in increasing MN survival and intramuscular axon branching. Together with previous reports, we also provide evidence consistent with a transition between the embryonic/fetal form to the adult form of muscle nAChRs in chicken that involves the loss of the gamma subunit in the adult receptor. We conclude that selective inhibition of the embryonic/fetal form of the chicken muscle nAChR is sufficient to rescue MNs from PCD without any involvement of neuronal nAChRs. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008