The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle-specific nicotinic acetylcholine receptor.
The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle-specific nicotinic acetylcholine receptor.
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通过胎儿肌肉特异性烟碱乙酰胆碱受体的选择性抑制剂来拯救发育中的鸟类运动神经元免于程序性细胞死亡。
DOI：
10.1002/dneu.20636
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发表时间：
2008
影响因子：
3
通讯作者：
Teichert,RussellW
中科院分区：
文献类型：
--
作者：
Oppenheim,RonaldW;Caldero,Jordi;Cuitat,Doloros;Esquerda,Josep;McArdle,JosephJ;Olivera,BaldomeroM;Prevette,David;Teichert,RussellW
为了确定在神经肌肉功能降低后，鸡胚中从程序性细胞死亡（PCD）中拯救发育中的运动神经元（MNS）是否涉及肌肉或神经元烟碱乙酰胆碱受体（nAChR），我们采用了一种新型锥螺毒素α A-OLVA，其选择性地拮抗胚胎/胎儿形式的肌肉nAChR。结果表明，α A-OLVA在降低神经肌肉功能方面几乎与箭毒或α-银环蛇毒素（α-BTX）一样有效，并且在增加MN存活和肌内轴突分支方面同样有效。与以前的报告一起，我们还提供了与鸡的肌肉nAChRs的胚胎/胎儿形式到成人形式之间的过渡相一致的证据，该过渡涉及成人受体中γ亚基的丢失。我们的结论是，选择性抑制胚胎/胎儿形式的鸡肌肉nAChR是足以拯救MN从PCD没有任何参与的神经元nAChRs。© 2008 Wiley Periodicals，Inc.开发神经生物学，2008年
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