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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >β-Neuregulin-1 is required for the in vivo development of functional Ca~2+-activated K~+ channels in parasympathetic neurons
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β-Neuregulin-1 is required for the in vivo development of functional Ca~2+-activated K~+ channels in parasympathetic neurons

机译：副交感神经元体内功能性Ca〜2 +激活的K〜+通道的体内发育需要β-Neuregulin-1

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摘要

The development of functional Ca~2+-activated K~+ channels (Kc_a) in chick ciliary ganglion (CG) neurons requires interactions with afferent preganglionic nerve terminals. Here we show that the essential preganglionic differentiation factor is an isoform of β-neuregulin-1. β-Neuregulin-1 transcripts are expressed in the midbrain preganglionic Edinger-Westphal nucleus at developmen- tal stages that coincide with or precede the normal onset of macroscopic Kc_a in CG neurons. Injection of β-neuregulin-1 peptide into the brains of developing embryos evoked a robust stimulation of functional Kc_a channels at stages before the normal appearance of these channels in CG neurons developing in vivo. Conversely. injection of a neutralizing antiserum specific for β-neuregulin-1 inhibited the development of Kc_a channels in CG neurons. Low concentrations of β-neuregulin-1 evoked a robust increase in whole-cell Kc_a in CG neurons cocultured with iris target tissues. By contrast, Culturing CG neurons with iris cells or low concentrations of β-neuregulin-1 by themselves was insufficient to stimulate Kc_a. These data Suggest that the preganglionic factor required for the development of Kc_a in ciliary ganglion neurons is an isoform of β-neuregulin-1. and that this factor acts in concert with target- derived trophic molecules to regulate the differentiation of excitability.
机译：鸡睫状神经节（CG）神经元中的功能性Ca〜2 +激活的K〜+通道（Kc_a）的发育需要与传入的神经节前神经末梢相互作用。在这里，我们显示必需的神经节前分化因子是β-神经调节蛋白-1的同工型。 β-Neuregulin-1转录本在中脑神经节前的爱丁格-韦斯特法尔核中表达，处于发育阶段，与CG神经元中宏观Kc_a的正常发作相吻合或在此之前发生。将β-神经调节蛋白-1肽注射到发育中的胚胎的大脑中，可以在体内发育的CG神经元正常出现这些阶段之前，刺激这些功能性Kc_a通道。反过来。注射特异性针对β-神经调节蛋白1的中和抗血清抑制了CG神经元中Kc_a通道的发育。低浓度的β-神经调节蛋白1引起与虹膜靶组织共培养的CG神经元全细胞Kc_a的强劲增加。相反，用虹膜细胞或低浓度的β-神经调节蛋白1培养CG神经元不足以刺激Kc_a。这些数据表明，在睫状神经节神经元中形成Kc_a所需的神经节前因子是β-神经调节蛋白-1的同工型。并且该因子与靶标衍生的营养分子协同作用，以调节兴奋性的差异。

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