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首页> 外文期刊>The European Journal of Neuroscience >Modifications of intracellular Ca2+ signalling during nerve growth factor-induced neuronal differentiation of rat adrenal chromaffin cells.
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Modifications of intracellular Ca2+ signalling during nerve growth factor-induced neuronal differentiation of rat adrenal chromaffin cells.

机译：神经生长因子诱导的大鼠肾上腺嗜铬细胞神经元分化过程中细胞内Ca2 +信号传导的修饰。

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摘要

Postnatal sympathetic neurons (SNs) and chromaffin cells (CCs) derive from neural crest precursors. CCs can differentiate in vitro into SN-like cells after nerve growth factor (NGF) exposure. This study examines changes of intracellular Ca2+ homeostasis and dynamics of CCs under conditions that promote a neuronal phenotype. Spontaneous Ca2+ fluctuations, a frequent observation in early cultures of CCs, diminished after > 10 days in vitro in control cells and ceased in NGF-treated ones. At the same time, Ca2+ rises resulting from entry upon membrane depolarization, gradually increased both their size and peak d[Ca2+]i/dt, resembling those recorded in SNs. Concomitantly, caffeine-induced Ca2+ rises, resulting from Ca2+ release from intracellular stores, increased their size and their peak d[Ca2+]i/dt by > 1000%, and developed transient and sustained release components, similar to those of SNs. The transient component, linked to regenerative Ca2+ release, appeared after > 10 days of NGF treatment, suggesting a delayed steep enhancement of Ca2+-induced Ca2+ release (CICR). Immunostaining showed that proteins coded by the three known isoforms of ryanodine receptors (RyRs) are present in CCs, but that only RyR2 increased significantly after NGF treatment. Since the transient release component increased more steeply than RyR2 immunostaining, we suggest that the development of robust CICR requires both an increased expression of RyRs and more efficient functional coupling among them. NGF-induced transdifferentiation of chromaffin cells involves the enhancement of both voltage-gated Ca2+ influx and Ca2+ release from intracellular stores. These modifications are likely to complement the extensive morphological and functional reorganization required for the replacement of the endocrine phenotype with the neuronal one.
机译：产后交感神经元（SN）和嗜铬细胞（CC）来自神经c前体。暴露于神经生长因子（NGF）后，CC可以在体外分化为SN样细胞。这项研究检查了在促进神经元表型的条件下细胞内Ca2 +稳态的变化和CC的动态。自发的Ca2 +波动是CC早期培养中经常观察到的现象，在对照细胞中体外> 10天后，其减弱了，而在经过NGF处理的细胞中则停止了。同时，Ca2 +会因膜去极化进入而上升，并逐渐增加其大小和峰d [Ca2 +] i / dt，类似于SN中记录的峰。伴随地，咖啡因诱导的Ca2 +升高是由于细胞内存储中Ca2 +的释放，其大小增加和其d [Ca2 +] i / dt峰值增加> 1000％，并形成了类似于SN的瞬时和持续释放成分。 NGF处理> 10天后，出现了与再生Ca2 +释放相关的瞬时成分，这表明Ca2 +诱导的Ca2 +释放（CICR）的延迟陡峭增强。免疫染色显示，在CC中存在由ryanodine受体（RyRs）的三种已知同工型编码的蛋白质，但NGF处理后仅RyR2显着增加。由于瞬时释放成分比RyR2免疫染色的增加要陡得多，因此我们建议开发健壮的CICR既需要RyRs的表达增加，也需要它们之间更有效的功能偶联。 NGF诱导的嗜铬细胞的转分化涉及电压门控的Ca2 +内流和细胞内存储中Ca2 +释放的增强。这些修饰很可能补充用神经元替代内分泌表型所需的广泛的形态和功能重组。

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