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Войти в исследования Experimental neurology · 2026
Focal ischemic stroke impairs REM sleep and inhibits c-Fos expression of SST neuron in EP of male rats.
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Xiong Ying-Qi, Yin Dan, Qi Wen-Bin, Zhao Chuan-Rui, Wang Xuan, Yan Xiao-Wei, Yang Zhang, Zhang Ju, Li Yi-Xin, Xia Bai-Juan, Li Rong-Rong
Аннотация
PURPOSE: The basal ganglia contribute to sleep-wake regulation and are vulnerable to ischemic stroke. Specifically, the striatum, as an upstream input region, appears critically involved, since rapid eye movement (REM) sleep disruption occurs in both extensive (cortex and striatum) and focal striatal infarcts. Nonetheless, the post-stroke dynamics of REM sleep disturbances and their neural targets remain unclear, largely due to the technical limitations in animal models and complexity of stroke outcomes.
METHODS: We modified the transient middle cerebral artery occlusion model in rats to induce focal ischemic stroke which mainly located in dorsal striatum. Sleep-wake cycles were monitored for six consecutive days using in vivo electrophysiology. Immunofluorescence for detecting c-Fos positive cells was performed in the output nuclei of the basal ganglia.
RESULTS: Focal ischemic stroke persistently decreased REM sleep in rats during the light phase, manifesting as reduced REM sleep proportion, altered stage transitions, and prolonged latency. This was accompanied by decreased REM sleep-related oscillatory power in the dorsal striatum. Stroke additionally impaired the memory performance in rats. Further investigation into the neural mechanisms revealed that the entopeduncular nucleus (EP) is a candidate target of REM sleep reduction. Specifically, the decreased c-Fos expression occurred predominantly within somatostatin neurons, but not parvalbumin neurons in EP.
CONCLUSION: We hypothesize that striatal dysfunction contributes significantly to post-stroke REM sleep disturbances, and may do so via reduced c-Fos expression in EP SST+ neurons.
METHODS: We modified the transient middle cerebral artery occlusion model in rats to induce focal ischemic stroke which mainly located in dorsal striatum. Sleep-wake cycles were monitored for six consecutive days using in vivo electrophysiology. Immunofluorescence for detecting c-Fos positive cells was performed in the output nuclei of the basal ganglia.
RESULTS: Focal ischemic stroke persistently decreased REM sleep in rats during the light phase, manifesting as reduced REM sleep proportion, altered stage transitions, and prolonged latency. This was accompanied by decreased REM sleep-related oscillatory power in the dorsal striatum. Stroke additionally impaired the memory performance in rats. Further investigation into the neural mechanisms revealed that the entopeduncular nucleus (EP) is a candidate target of REM sleep reduction. Specifically, the decreased c-Fos expression occurred predominantly within somatostatin neurons, but not parvalbumin neurons in EP.
CONCLUSION: We hypothesize that striatal dysfunction contributes significantly to post-stroke REM sleep disturbances, and may do so via reduced c-Fos expression in EP SST+ neurons.