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The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle‐specific nicotinic acetylcholine receptor
Author(s) -
Oppenheim Ronald W.,
Calderó Jordi,
Cuitat Doloros,
Esquerda Josep,
McArdle Joseph J.,
Olivera Baldomero M.,
Prevette David,
Teichert Russell W.
Publication year - 2008
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.20636
Subject(s) - biology , acetylcholine receptor , curare , nicotinic acetylcholine receptor , nicotinic agonist , neuromuscular junction , neuroscience , axon , embryonic stem cell , microbiology and biotechnology , receptor , acetylcholine , fetus , endocrinology , biochemistry , genetics , pregnancy , gene
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