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.
Highlights
The complex relationship between specific hippocampal oscillation frequency deficit and cognitive dysfunction in the ischemic brain is unclear
Reduction in hippocampal local field potential (LFPs) cross-frequency coupling (CFC) between theta and gamma is associated with impaired long-term potentiation (LTP) in the anesthetized rat with transient global cerebral ischemia[8]
To demonstrate the effects of different frequencies of light flicker on CA1 oscillations, local field potentials (LFPs) were recorded in mice implanted with a four-electrode array into the CA1 stratum pyramidale layer (Fig. 1a), followed by treatment with 10 Hz, 30 Hz, 40 Hz, 50 Hz, 80 Hz, arrhythmic frequency, or without light flicker light flicker (Fig. 1b–d and Supplementary Fig. 1j–m)
Summary
The complex relationship between specific hippocampal oscillation frequency deficit and cognitive dysfunction in the ischemic brain is unclear. 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. 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. We show rhythmic 30–50 Hz light flicker can restore hippocampal CA1 low gamma oscillation and protect ischemic CA1 neurons through a mechanism requiring RGS12-regulated N-type CaV2.2 voltage-gated calcium channels (N-VGCC)-dependent enhancement of synaptic plasticity
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