Electroacupuncture improves neurocognitive impairment induced by chronic sleep deprivation: an experimental study...

Normal sleep rhythms are crucial for hippocampus-dependent advanced cognitive functions. Chronic sleep deprivation (CSD) impairs hippocampal neurogenesis and structure, leading to neurocognitive deficits. Electro-nape-acupuncture (ENA) at bilateral Fengchi (GB20) and Gongxue (Extra) is a specialized acupuncture technique for treating insomnia, amnesia, and other brain-originated diseases. This study aims to investigate whether ENA improves CSD-induced cognitive impairment by regulating neurogenesis and synaptic plasticity in the hippocampus.

The modified multi-platform water environment method was used to establish the CSD model. Electroacupuncture or sham electroacupuncture was used to treat bilateral cervical acupoints (Fengchi and Gongxue) for 20 min, once a day for 14 days. The Morris water maze experiment evaluated spatial learning and memory in rats, and the new object recognition experiment evaluated recognition memory. Immunofluorescence (IF) staining and Western Blot (WB) were used to detect the expression levels of the hippocampal neurogenesis markers, doublecortin (DCX) and Ki-67. Golgi-Cox staining and transmission electron microscopy were used to observe the changes in neurons and synaptic plasticity in the dentate gyrus (DG) of the hippocampus.

Neurocognitive impairment induced by CSD is associated with abnormal changes in hippocampal neurogenesis and synaptic plasticity. The results of IF and WB showed that the protein expressions of DCX and Ki-67 in the hippocampus of CSD rats were significantly decreased. Transmission electron microscopy revealed that in the DG region of the hippocampus of CSD rats, the synaptic density and the thickness of the postsynaptic density membrane decreased, while the synaptic cleft width increased. Golgi staining showed that the density of dendritic spines in the DG area of the hippocampus in CSD rats decreased significantly, especially mushroom-shaped dendritic spines. ENA can enhance spatial learning and memory, as well as recognition memory, induced by CSD, and effectively reverse the abnormal changes in neurogenesis and synaptic plasticity in the DG region of the hippocampus.

In male Wistar rats, ENA improves neurocognitive function by promoting neurogenesis in the hippocampal dentate gyrus and restoring synaptic plasticity, thereby reconstructing neural memory circuits. ENA therapy offers a new strategy for treating cognitive impairments related to chronic sleep deprivation in males, and holds potential significance for the clinical management of cognitive impairment diseases.