Center for Integrative Neuroscience, Department of Physiology, University of California, 675 Nelson Rising Road, San Francisco, CA 94158, USA.
Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA; MSTP/Neuroscience graduate Program, Stony Brook University, Stony Brook, NY 11790, USA.
Cell. 2014 Mar 13;156(6):1139-1152. doi: 10.1016/j.cell.2014.01.050.
The brain's response to sensory input is strikingly modulated by behavioral state. Notably, the visual response of mouse primary visual cortex (V1) is enhanced by locomotion, a tractable and accessible example of a time-locked change in cortical state. The neural circuits that transmit behavioral state to sensory cortex to produce this modulation are unknown. In vivo calcium imaging of behaving animals revealed that locomotion activates vasoactive intestinal peptide (VIP)-positive neurons in mouse V1 independent of visual stimulation and largely through nicotinic inputs from basal forebrain. Optogenetic activation of VIP neurons increased V1 visual responses in stationary awake mice, artificially mimicking the effect of locomotion, and photolytic damage of VIP neurons abolished the enhancement of V1 responses by locomotion. These findings establish a cortical circuit for the enhancement of visual response by locomotion and provide a potential common circuit for the modulation of sensory processing by behavioral state.
大脑对感觉输入的反应受到行为状态的显著调节。值得注意的是,小鼠初级视觉皮层 (V1) 的视觉反应会因运动而增强,这是皮质状态时间锁定变化的一个易于处理和可访问的例子。将行为状态传递到感觉皮层以产生这种调制的神经回路尚不清楚。对行为动物的活体钙成像显示,运动独立于视觉刺激激活小鼠 V1 中的血管活性肠肽 (VIP) 阳性神经元,主要通过基底前脑的烟碱能输入。光遗传学激活 VIP 神经元可增加静止清醒小鼠 V1 的视觉反应,人为模拟运动的效果,而 VIP 神经元的光化学损伤则消除了运动对 V1 反应的增强。这些发现确立了运动增强视觉反应的皮质回路,并为行为状态对感觉处理的调制提供了一个潜在的共同回路。