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首页> 外文期刊>BMC Neuroscience >Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of Ca V 1 channels
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Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of Ca V 1 channels

机译：纹状体快速爆发中神经元中的钙电流：Ca V 1通道的多巴胺能调节

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Striatal fast-spiking interneurons (FSI) are a subset of GABAergic cells that express calcium-binding protein parvalbumin (PV). They provide feed-forward inhibition to striatal projection neurons (SPNs), receive cortical, thalamic and dopaminergic inputs and are coupled together by electrical and chemical synapses, being important components of the striatal circuitry. It is known that dopamine (DA) depolarizes FSI via D1-class DA receptors, but no studies about the ionic mechanism of this action have been reported. Here we ask about the ion channels that are the effectors of DA actions. This work studies their Ca2+ currents. Whole-cell recordings in acutely dissociated and identified FSI from PV-Cre transgenic mice were used to show that FSI express an array of voltage gated Ca2+ channel classes: CaV1, CaV2.1, CaV2.2, CaV2.3 and CaV3. However, CaV1 Ca2+ channel carries most of the whole-cell Ca2+ current in FSI. Activation of D1-like class of DA receptors by the D1-receptor selective agonist SKF-81297 (SKF) enhances whole-cell Ca2+ currents through CaV1 channels modulation. A previous block of CaV1 channels with nicardipine occludes the action of the DA-agonist, suggesting that no other Ca2+ channel is modulated by D1-receptor activation. Bath application of SKF in brain slices increases the firing rate and activity of FSI as measured with both whole-cell and Ca2+ imaging recordings. These actions are reduced by nicardipine. The present work discloses one final effector of DA modulation in FSI. We conclude that the facilitatory action of DA in FSI is in part due to CaV1 Ca2+ channels positive modulation.
机译：纹状体快速加标中枢神经元（FSI）是表达钙结合蛋白小白蛋白（PV）的GABA能细胞的子集。它们对纹状体投射神经元（SPN）提供前馈抑制，接收皮质，丘脑和多巴胺能输入，并通过电和化学突触耦合在一起，这是纹状体电路的重要组成部分。众所周知，多巴胺（DA）通过D1类DA受体使FSI去极化，但是尚未见有关此作用的离子机制的研究。在这里，我们询问有关DA作用的离子通道。这项工作研究其Ca2 +电流。从PV-Cre转基因小鼠中急性分离和鉴定的FSI中的全细胞记录用于显示FSI表达一系列电压门控Ca2 +通道类别：CaV1，CaV2.1，CaV2.2，CaV2.3和CaV3。但是，CaV1 Ca2 +通道在FSI中承载了大部分的全细胞Ca2 +电流。 D1受体选择性激动剂SKF-81297（SKF）对D1类DA受体的激活通过CaV1通道调节增强了全细胞Ca2 +电流。先前带有尼卡地平的CaV1通道阻滞了DA激动剂的作用，表明D1受体激活没有其他Ca2 +通道被调节。如在全细胞和Ca2 +成像记录中所测量的，将SKF浸浴在脑切片中可提高FSI的放电率和活性。尼卡地平可减少这些作用。本工作公开了FSI中DA调制的一种最终效应器。我们得出结论，在FSI中DA的促进作用部分归因于CaV1 Ca2 +通道的正调制。

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