Increasing evidence has shown that voltage-gated L-type Ca²⁺ channels (LTCCs) are crucial for neurodevelopmental events, including neuronal differentiation/migration and neurite morphogenesis/extension. However, the time course of their functional maturation during the development of excitatory neurons remains unknown. Using a combination of fluorescence in situ hybridization and in utero electroporation-based labeling, we found that the transcripts of Cacna1c and Cacna1d, which encode the LTCC pore-forming subunits, were upregulated in the intermediate zone (IZ) during radial migration. Ca²⁺ imaging using GCaMP6s in acute brain slices showed spontaneous Ca²⁺ transients in migrating neurons throughout the IZ. Neurons in the IZ upper layer, especially in the multipolar-to-bipolar transition layer (TL), exhibited more frequent Ca²⁺ transients than adjacent layers and responded to FPL64176, a potent activator of LTCC. Consistently, nimodipine, an LTCC blocker, inhibited spontaneous Ca²⁺ transients in neurons in the TL. Collectively, we showed a hitherto unknown increased prevalence of LTCC-dependent Ca²⁺ transients in the TL of the IZ upper layer during the radial migration of excitatory neurons, which could be essential for the regulation of Ca²⁺-dependent neurodevelopmental processes.

越来越多的证据表明，电压门控 L 型 Ca ²⁺通道 (LTCC) 对神经发育事件至关重要，包括神经元分化/迁移和轴突形态发生/延伸。然而，它们在兴奋性神经元发育过程中功能成熟的时间过程仍然未知。使用荧光原位杂交和基于子宫内电穿孔的标记的组合，我们发现编码 LTCC 成孔亚基的Cacna1c和Cacna1d的转录本在径向迁移期间在中间区 (IZ) 中上调。在急性脑切片中使用 GCaMP6s 的Ca ²⁺成像显示自发性 Ca ²⁺整个 IZ 中迁移神经元的瞬态。IZ 上层的神经元，尤其是多极到双极过渡层 (TL) 中的神经元，表现出比相邻层更频繁的 Ca ²⁺瞬变，并对 FPL64176（LTCC 的一种有效激活剂）做出响应。始终如一地，尼莫地平（一种 LTCC 阻滞剂）抑制了 TL 神经元中的自发 Ca ²⁺瞬变。总的来说，我们发现在兴奋性神经元径向迁移期间，IZ 上层 TL中 LTCC 依赖性 Ca ²⁺瞬变的发生率前所未有地增加，这可能对调节 Ca ²⁺依赖性神经发育过程至关重要。