mGlu1α-dependent recruitment of excitatory GABAergic input to neocortical Cajal-Retzius cells.
mGlu1α-dependent recruitment of excitatory GABAergic input to neocortical Cajal-Retzius cells.
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DOI：
10.1016/j.neuropharm.2012.04.025
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发表时间：
2012-09
影响因子：
4.7
通讯作者：
Maccaferri G
中科院分区：
文献类型：
--
作者：
Cosgrove KE;Maccaferri G
Cajal-Retzius 细胞被认为在皮质发育中发挥重要作用，并且主要接收由 GABAA 受体介导的自发 GABA 能输入。然而，突触释放的 GABA 对其兴奋性的影响以及自发 GABA 电流的细胞来源尚未确定。通过直接记录CXCR4-EGFP小鼠Cajal-Retzius细胞的电生理反应，我们发现GABA能输入可以触发超阈值反应，并且I组激动剂DHPG对mGlu1α受体的药理学激活有力地增加了自发GABA能电流的频率。这些效应似乎是由网络机制介导的，因为通过手术将 I 层与下层断开以及将切片暴露于 TTX 完全阻止了对 DHPG 的反应。我们提出，观察到的 DHPG 效应背后的细胞来源是 I 层靶向 Martinotti 样中间神经元，我们显示其表达功能组 I mGluR，并在早期发育阶段就以超阈值去极化对 DHPG 做出反应。总之，我们的工作表明，增强谷氨酸释放的条件可能在早期发育阶段对于招募 mGlu1α 依赖性微电路至关重要，从而导致 Cajal-Retzius 细胞的激活。
Cajal-Retzius cells are thought to play an important role for cortical development, and receive primarily spontaneous GABAergic input mediated by GABAA receptors. However, neither the effects of synaptically-released GABA on their excitability nor the cellular source(s) of spontaneous GABAergic currents have been yet determined. By directly recording electrophysiological responses from identified Cajal-Retzius cells of the CXCR4-EGFP mouse, we show that GABAergic input can trigger supra-threshold responses, and that the pharmacological activation of mGlu1α receptors with the group I agonist DHPG powerfully increases the frequency of spontaneous GABAergic currents. These effects appeared mediated by a network mechanism, because responses to DHPG were completely prevented both by surgical disconnection of layer I from lower layers and by exposure of slices to TTX. We propose that the cellular source underlying the observed effect of DHPG are layer I-targeting Martinotti-like interneurons, which we show express functional group I mGluRs and respond to DHPG with supra-threshold depolarization already at early developmental stages. In conclusion, our work suggests that conditions of enhanced glutamate release may be critical at early developmental stages for the recruitment of an mGlu1α-dependent micro-circuit, which then leads to the activation of Cajal-Retzius cells.
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