Calcium Signaling during Cortical Apical Dendrite Initiation: A Role for Cajal-Retzius Neurons.
Calcium Signaling during Cortical Apical Dendrite Initiation: A Role for Cajal-Retzius Neurons.
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DOI：
10.3390/ijms241612965
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发表时间：
2023-08-19
影响因子：
5.6
通讯作者：
Olson, Eric C.
中科院分区：
文献类型：
--
作者：
Enck, Joshua R.;Olson, Eric C.
皮层投射神经元（CPN）的顶树突是在迁移神经元完成迁移时由迁移神经元的前导过程产生的。这种转变发生在皮质边缘区（MZ），一个包含Cajal-Retzius神经元及其轴突投射的层。Cajal-Retzius神经元（CRN）以其在分泌Reelin中的关键作用而闻名，Reelin是一种控制发育中大脑许多区域中的树突发生和细胞定位的糖蛋白。在这项研究中，我们研究的可能性，CRNs在MZ可能会提供额外的信号到达CPNs，这可能会促进CPNs的成熟，从而塑造皮层的发展。我们使用整个胚胎半球外植体和多光子显微镜证实CRN显示细胞内钙瞬变的时间<1分钟和高振幅在早期皮质生成。相比之下，发育中的CPN并不表现出高幅度的钙瞬变，而是表现出细胞内钙的稳定增加，这种增加始于树枝状细胞起始时，即迁移CPN的主导过程遇到MZ时。CRN到CPN通信的可能存在被揭示的应用藜芦碱，钠通道激活剂，已被证明优先刺激更成熟的细胞在MZ在早期发育的时间。令人惊讶的是，藜芦碱的应用还引发CPN中的大的钙瞬变，其可以被阻断谷氨酸和甘氨酸受体活化的拮抗剂的混合物部分阻断。这些发现概述了一个模型，其中CRN自发活动触发谷氨酸和甘氨酸的释放，这些神经递质可以触发CPN细胞内钙离子升高。这些海拔开始作为CPNs启动树突状细胞，并继续在迁移后的细胞波。此外，我们发现，药理学阻断的amatergic信号中断迁移，而强制表达的细菌电压门控钙通道（CavMr）在迁移的神经元促进树突状细胞的生长和迁移逮捕。在早期发育过程中识别CRN到CPN信号提供了对以下观察的深入了解：许多自闭症相关基因编码突触蛋白，这些突触蛋白自相矛盾地在突触出现和功能回路建立之前就在发育中的皮质中表达。
The apical dendrite of a cortical projection neuron (CPN) is generated from the leading process of the migrating neuron as the neuron completes migration. This transformation occurs in the cortical marginal zone (MZ), a layer that contains the Cajal-Retzius neurons and their axonal projections. Cajal-Retzius neurons (CRNs) are well known for their critical role in secreting Reelin, a glycoprotein that controls dendritogenesis and cell positioning in many regions of the developing brain. In this study, we examine the possibility that CRNs in the MZ may provide additional signals to arriving CPNs, that may promote the maturation of CPNs and thus shape the development of the cortex. We use whole embryonic hemisphere explants and multiphoton microscopy to confirm that CRNs display intracellular calcium transients of <1-min duration and high amplitude during early corticogenesis. In contrast, developing CPNs do not show high-amplitude calcium transients, but instead show a steady increase in intracellular calcium that begins at the time of dendritic initiation, when the leading process of the migrating CPN is encountering the MZ. The possible existence of CRN to CPN communication was revealed by the application of veratridine, a sodium channel activator, which has been shown to preferentially stimulate more mature cells in the MZ at an early developmental time. Surprisingly, veratridine application also triggers large calcium transients in CPNs, which can be partially blocked by a cocktail of antagonists that block glutamate and glycine receptor activation. These findings outline a model in which CRN spontaneous activity triggers the release of glutamate and glycine, neurotransmitters that can trigger intracellular calcium elevations in CPNs. These elevations begin as CPNs initiate dendritogenesis and continue as waves in the post-migratory cells. Moreover, we show that the pharmacological blockade of glutamatergic signaling disrupts migration, while forced expression of a bacterial voltage-gated calcium channel (CavMr) in the migrating neurons promotes dendritic growth and migration arrest. The identification of CRN to CPN signaling during early development provides insight into the observation that many autism-linked genes encode synaptic proteins that, paradoxically, are expressed in the developing cortex well before the appearance of synapses and the establishment of functional circuits.
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影响因子：
8.8
作者：
Anstoz, Max;Lee, Sun Kyong;Maccaferri, Gianmaria
通讯作者：
Maccaferri, Gianmaria
影响因子：
5.7
作者：
Elorriaga，Vicente;Pierani，Alessandra;Causeret，Frederic
通讯作者：
Causeret，Frederic
影响因子：
2.9
作者：
Marín-Padilla M
通讯作者：
Marín-Padilla M
影响因子：
30.8
作者：
HIROTSUNE, S;TAKAHARA, T;HAYASHIZAKI, Y
通讯作者：
HAYASHIZAKI, Y
DOI：
10.1111/j.1365-2990.1985.tb00026.x
发表时间：
1985-01-01
影响因子：
5
作者：
FABREGUES, I;FERRER, I;GINER, P
通讯作者：
GINER, P