nNOS-expressing interneurons control basal and behaviorally evoked arterial dilation in somatosensory cortex of mice.
nNOS-expressing interneurons control basal and behaviorally evoked arterial dilation in somatosensory cortex of mice.
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DOI：
10.7554/elife.60533
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发表时间：
2020-10-05
期刊：
影响因子：
7.7
通讯作者：
Drew PJ
中科院分区：
文献类型：
--
作者：
Echagarruga CT;Gheres KW;Norwood JN;Drew PJ
皮质神经活动与局部动脉直径和血流量相关。然而，哪些神经元控制脑动脉的动力学还不清楚。我们解剖的细胞机制控制基底直径和诱发扩张皮层动脉清醒，头部固定的小鼠。运动驱动强大的动脉扩张，增加在当地的场电位（LFP）的伽玛波段功率，并增加在锥体和神经元型一氧化氮合酶（nNOS）表达的神经元钙信号。化学或药理学调制的整体神经活动向上或向下引起相应的增加或减少基底动脉直径。单独调制锥体神经元活动对基础或诱发动脉扩张的影响很小，尽管LFP有明显的变化。调节nNOS表达神经元的活性驱动了基底动脉和诱发动脉直径的变化，而群体神经活性没有相应的变化。
Cortical neural activity is coupled to local arterial diameter and blood flow. However, which neurons control the dynamics of cerebral arteries is not well understood. We dissected the cellular mechanisms controlling the basal diameter and evoked dilation in cortical arteries in awake, head-fixed mice. Locomotion drove robust arterial dilation, increases in gamma band power in the local field potential (LFP), and increases calcium signals in pyramidal and neuronal nitric oxide synthase (nNOS)-expressing neurons. Chemogenetic or pharmocological modulation of overall neural activity up or down caused corresponding increases or decreases in basal arterial diameter. Modulation of pyramidal neuron activity alone had little effect on basal or evoked arterial dilation, despite pronounced changes in the LFP. Modulation of the activity of nNOS-expressing neurons drove changes in the basal and evoked arterial diameter without corresponding changes in population neural activity.