快速棘突神经元提供爆发、钙和可塑性的前馈控制，以实现高效学习。
Fast-Spiking Interneurons Supply Feedforward Control of Bursting, Calcium, and Plasticity for Efficient Learning.
机构信息
Gladstone Institutes, San Francisco, CA 94158, USA.
Department of Neurology, UCSF, San Francisco, CA 94158, USA; Kavli Institute for Fundamental Neuroscience, UCSF, San Francisco, CA 94158, USA; UCSF Weill Institute for Neurosciences, UCSF, San Francisco, CA 94158, USA.
出版信息
Cell. 2018 Feb 8;172(4):683-695.e15. doi: 10.1016/j.cell.2018.01.005.
Fast-spiking interneurons (FSIs) are a prominent class of forebrain GABAergic cells implicated in two seemingly independent network functions: gain control and network plasticity. Little is known, however, about how these roles interact. Here, we use a combination of cell-type-specific ablation, optogenetics, electrophysiology, imaging, and behavior to describe a unified mechanism by which striatal FSIs control burst firing, calcium influx, and synaptic plasticity in neighboring medium spiny projection neurons (MSNs). In vivo silencing of FSIs increased bursting, calcium transients, and AMPA/NMDA ratios in MSNs. In a motor sequence task, FSI silencing increased the frequency of calcium transients but reduced the specificity with which transients aligned to individual task events. Consistent with this, ablation of FSIs disrupted the acquisition of striatum-dependent egocentric learning strategies. Together, our data support a model in which feedforward inhibition from FSIs temporally restricts MSN bursting and calcium-dependent synaptic plasticity to facilitate striatum-dependent sequence learning.
快速棘突神经元（FSIs）是前脑 GABA 能神经元中的一个重要类别，其涉及两种看似独立的网络功能：增益控制和网络可塑性。然而，关于这些角色如何相互作用，我们知之甚少。在这里，我们使用细胞类型特异性消融、光遗传学、电生理学、成像和行为相结合的方法，描述了纹状体 FSIs 控制邻近的中等棘突投射神经元（MSNs）爆发性放电、钙内流和突触可塑性的统一机制。在体内沉默 FSIs 会增加 MSNs 的爆发、钙瞬变和 AMPA/NMDA 比值。在运动序列任务中，FSI 沉默增加了钙瞬变的频率，但降低了瞬变与单个任务事件对齐的特异性。与此一致的是，FSIs 的消融破坏了纹状体依赖的自我中心学习策略的获得。总的来说，我们的数据支持这样一种模型，即来自 FSIs 的前馈抑制在时间上限制 MSN 的爆发和钙依赖性突触可塑性，以促进纹状体依赖的序列学习。
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