PDF(Pubmed)
Abstract：
BACKGROUND: Tooth loss is closely related to cognitive impairment, especially affecting cognitive functions involving hippocampus. The most well-known function of the hippocampus is learning and memory, and the mechanism behind is neuroplasticity, which strongly depends on the level of brain-derived neurotrophic factor (BDNF). While research has delved into the possible mechanisms behind the loss of teeth leading to cognitive dysfunction, there are few studies on the plasticity of sensory neural pathway after tooth loss, and the changes in related indicators of synaptic plasticity still need to be further explored.
METHODS: In this study, the bilateral maxillary molars were extracted in Sprague-Dawley rats of two age ranges (young and middle age) to establish occlusal support loss model; then, the spatial cognition was tested by Morris Water Maze (MWM). Quantitative real-time PCR (qPCR) and Western Blotting (WB) were used to detect BDNF, AKT, and functional proteins (viz., PSD95 and NMDAR) of hippocampal synapses. Golgi staining was used to observe changes in ascending nerve pathway. IF was used to confirm the location of BDNF and AKT expressed in hippocampus.
RESULTS: MWM showed that the spatial cognitive level of rats dropped after occlusal support loss. qPCR, WB, and IF suggested that the BDNF/AKT pathway was down-regulated in the hippocampus. Golgi staining showed the neurons of ascending sensory pathway decreased in numbers.
CONCLUSIONS: Occlusal support loss caused plastic changes in ascending nerve pathway and induced cognitive impairment in rats by down-regulating BDNF and synaptic plasticity.
METHODS: In this study, the bilateral maxillary molars were extracted in Sprague-Dawley rats of two age ranges (young and middle age) to establish occlusal support loss model; then, the spatial cognition was tested by Morris Water Maze (MWM). Quantitative real-time PCR (qPCR) and Western Blotting (WB) were used to detect BDNF, AKT, and functional proteins (viz., PSD95 and NMDAR) of hippocampal synapses. Golgi staining was used to observe changes in ascending nerve pathway. IF was used to confirm the location of BDNF and AKT expressed in hippocampus.
RESULTS: MWM showed that the spatial cognitive level of rats dropped after occlusal support loss. qPCR, WB, and IF suggested that the BDNF/AKT pathway was down-regulated in the hippocampus. Golgi staining showed the neurons of ascending sensory pathway decreased in numbers.
CONCLUSIONS: Occlusal support loss caused plastic changes in ascending nerve pathway and induced cognitive impairment in rats by down-regulating BDNF and synaptic plasticity.
摘要：
背景：牙齿缺失与认知障碍密切相关，尤其是影响海马的认知功能。海马最著名的功能是学习和记忆，背后的机制是神经可塑性，这在很大程度上取决于脑源性神经营养因子（BDNF）的水平。虽然研究已经深入研究了牙齿脱落导致认知功能障碍的可能机制，关于牙齿脱落后感觉神经通路可塑性的研究很少，突触可塑性相关指标的变化仍需进一步探讨。
方法：在本研究中，拔除两个年龄范围(青年和中年)的Sprague-Dawley大鼠双侧上颌磨牙，建立咬合支持丢失模型；空间认知通过莫里斯水迷宫（MWM）进行测试。采用实时定量PCR(qPCR)和蛋白质印迹法(WB)检测BDNF,AKT,和功能性蛋白质(即,海马突触的PSD95和NMDAR）。高尔基染色观察上行神经通路的变化。IF用于确认海马中表达的BDNF和AKT的位置。
结果：MWM显示，失去咬合支持后，大鼠的空间认知水平下降。qPCR,WB,和IF提示海马中BDNF/AKT通路下调。高尔基染色显示上升感觉通路的神经元数量减少。
结论：咬合支持缺失通过下调BDNF和突触可塑性，导致大鼠上行神经通路的可塑性改变，并导致认知功能障碍。
方法：在本研究中，拔除两个年龄范围(青年和中年)的Sprague-Dawley大鼠双侧上颌磨牙，建立咬合支持丢失模型；空间认知通过莫里斯水迷宫（MWM）进行测试。采用实时定量PCR(qPCR)和蛋白质印迹法(WB)检测BDNF,AKT,和功能性蛋白质(即,海马突触的PSD95和NMDAR）。高尔基染色观察上行神经通路的变化。IF用于确认海马中表达的BDNF和AKT的位置。
结果：MWM显示，失去咬合支持后，大鼠的空间认知水平下降。qPCR,WB,和IF提示海马中BDNF/AKT通路下调。高尔基染色显示上升感觉通路的神经元数量减少。
结论：咬合支持缺失通过下调BDNF和突触可塑性，导致大鼠上行神经通路的可塑性改变，并导致认知功能障碍。
