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首页> 外文期刊>The European Journal of Neuroscience >Brain-derived neurotrophic factor controls functional differentiation and microcircuit formation of selectively isolated fast-spiking GABAergic interneurons.
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Brain-derived neurotrophic factor controls functional differentiation and microcircuit formation of selectively isolated fast-spiking GABAergic interneurons.

机译：脑源性神经营养因子控制选择性分离的快速加标的GABA能中间神经元的功能分化和微电路形成。

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Abstract GABAergic interneurons with high-frequency firing, fast-spiking (FS) cells, form synapses on perisomatic regions of principal cells in the neocortex and hippocampus to control the excitability of cortical networks. Brain-derived neurotrophic factor (BDNF) is essential for the differentiation of multiple interneuron subtypes and the formation of their synaptic contacts. Here, we examined whether BDNF, alone or in conjunction with sustained KCl-induced depolarization, drives functional FS cell differentiation and the formation of inhibitory microcircuits. Homogeneous FS cell cultures were established by target-specific isolation using the voltage-gated potassium channel 3.1b subunit as the selection marker. Isolated FS cells expressed parvalbumin, were surrounded by perineuronal nets, formed immature inhibitory connections and generated slow action potentials at 12 days in vitro. Brain-derived neurotrophic factor (BDNF) promoted FS cell differentiation by increasing the somatic diameter, dendritic branching and the frequency of action potential firing. In addition, BDNF treatment led to a significant up-regulation of synaptophysin and vesicular GABA transporter expression, components of the synaptic machinery critical for GABA release, which was paralleled by an increase in synaptic strength. Long-term membrane depolarization alone was detrimental to dendritic branching. However, we observed that BDNF and KCl exerted additive effects, as reflected by the significantly accelerated maturation of synaptic contacts and high discharge frequencies, and was required for the formation of reciprocal connections between FS cells. Our results show that BDNF, along with membrane depolarization, is critical for FS cells to establish inhibitory circuitries during corticogenesis.
机译：摘要具有高频放电，快速放电（FS）细胞的GABA能神经元在新皮层和海马的主要细胞的胞界区域形成突触，以控制皮质网络的兴奋性。脑源性神经营养因子（BDNF）对于多种中间神经元亚型的分化及其突触接触的形成至关重要。在这里，我们检查了BDNF是单独还是与持续的KCl诱导的去极化一起驱动功能性FS细胞分化和抑制性微电路的形成。通过使用电压门控钾通道3.1b亚基作为选择标记的靶标特异性分离建立了同质FS细胞培养物。分离的FS细胞表达小白蛋白，被神经周围神经网络包围，形成不成熟的抑制性连接，并在体外第12天产生缓慢的动作电位。脑源性神经营养因子（BDNF）通过增加体细胞直径，树突分支和动作电位激发的频率来促进FS细胞分化。此外，BDNF治疗导致突触素和水泡GABA转运蛋白表达的显着上调，这是对GABA释放至关重要的突触机制的组成部分，同时突触强度增加。单独的长期膜去极化对树突分支有害。但是，我们观察到BDNF和KCl发挥了累加作用，这由突触接触的成熟加速和高放电频率反映出来，并且是FS细胞之间相互连接所必需的。我们的研究结果表明，BDNF以及膜去极化对FS细胞在皮质形成过程中建立抑制性回路至关重要。

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