Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Neuron. 2021 Mar 17;109(6):997-1012.e9. doi: 10.1016/j.neuron.2021.01.003. Epub 2021 Feb 1.
Interneurons expressing cholecystokinin (CCK) and parvalbumin (PV) constitute two key GABAergic controllers of hippocampal pyramidal cell output. Although the temporally precise and millisecond-scale inhibitory regulation of neuronal ensembles delivered by PV interneurons is well established, the in vivo recruitment patterns of CCK-expressing basket cell (BC) populations has remained unknown. We show in the CA1 of the mouse hippocampus that the activity of CCK BCs inversely scales with both PV and pyramidal cell activity at the behaviorally relevant timescales of seconds. Intervention experiments indicated that the inverse coupling of CCK and PV GABAergic systems arises through a mechanism involving powerful inhibitory control of CCK BCs by PV cells. The tightly coupled complementarity of two key microcircuit regulatory modules demonstrates a novel form of brain-state-specific segregation of inhibition during spontaneous behavior.
表达胆囊收缩素 (CCK) 和小白蛋白 (PV) 的中间神经元构成了海马锥体细胞输出的两个关键 GABA 能控制器。尽管 PV 中间神经元提供的神经元集合的时间精确且毫秒级的抑制调节已经得到充分证实,但 CCK 表达篮状细胞 (BC) 群体的体内募集模式仍然未知。我们在小鼠海马体的 CA1 区中表明,在与行为相关的秒级时间尺度上,CCK BC 的活动与 PV 和锥体细胞的活动呈反比。干预实验表明,CCK 和 PV GABA 能系统的反向耦合是通过一种机制产生的,该机制涉及 PV 细胞对 CCK BC 进行强大的抑制控制。两个关键微电路调节模块的紧密耦合互补表明,在自发行为期间,抑制作用具有一种新的脑状态特异性分离形式。