Rhythmic light flicker rescues hippocampal low gamma and protects ischemic neurons by enhancing presynaptic plasticity

Lifeng Zheng, Mei Yu, Rui Lin, Yunxuan Wang, Zhan Zhuo, Ning Cheng, Mengzhen Wang, Yongqiang Tang, Liping Wang and Sheng-Tao Hou ()
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Lifeng Zheng: Southern University of Science and Technology
Mei Yu: Southern University of Science and Technology
Rui Lin: Southern University of Science and Technology
Yunxuan Wang: Southern University of Science and Technology
Zhan Zhuo: Southern University of Science and Technology
Ning Cheng: The Shenzhen Second People’s Hospital and the First Affiliated Hospital of Shenzhen University Health Science Center
Mengzhen Wang: Southern University of Science and Technology
Yongqiang Tang: Chinese Academy of Sciences
Liping Wang: Chinese Academy of Sciences
Sheng-Tao Hou: Southern University of Science and Technology

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract The complex relationship between specific hippocampal oscillation frequency deficit and cognitive dysfunction in the ischemic brain is unclear. Here, using a mouse two-vessel occlusion (2VO) cerebral ischemia model, we show that visual stimulation with a 40 Hz light flicker drove hippocampal CA1 slow gamma and restored 2VO-induced reduction in CA1 slow gamma power and theta-low gamma phase-amplitude coupling, but not those of the high gamma. Low gamma frequency lights at 30 Hz, 40 Hz, and 50 Hz, but not 10 Hz, 80 Hz, and arrhythmic frequency light, were protective against degenerating CA1 neurons after 2VO, demonstrating the importance of slow gamma in cognitive functions after cerebral ischemia. Mechanistically, 40 Hz light flicker enhanced RGS12-regulated CA3-CA1 presynaptic N-type calcium channel-dependent short-term synaptic plasticity and associated postsynaptic long term potentiation (LTP) after 2VO. These results support a causal relationship between CA1 slow gamma and cognitive dysfunctions in the ischemic brain.

Date: 2020
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DOI: 10.1038/s41467-020-16826-0

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