摘要
目的:探讨海马齿状回(DG)区小清蛋白阳性中间神经元(PV-INs)参与运动疲劳降低空间识别记忆的神经调控机制。方法:采用随机数字法将雄性SD大鼠分为对照组(Control)和运动疲劳组(Fatigue)。选用三级递增负荷跑台训练方案建立慢性力竭运动疲劳模型。利用新物体识别测试大鼠空间识别记忆能力,通过免疫荧光染色和免疫组化染色观察并量化大鼠海马DG区星形胶质细胞(AS)和PV-INs活性和数量,使用Western blot检测大鼠海马组织钙离子/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)磷酸化表达水平。结果:在新物体识别实验中,疲劳组大鼠对新物体的探索时间减少,新异物体识别指数显著低于对照组(P<0.01);免疫组织化学染色结果显示,疲劳组大鼠DG区PV-INs较对照组染色浅且数量少,纤维短小并且稀疏,细胞面密度以及平均光密度均显著低于对照组(P<0.01);免疫荧光染色结果显示,疲劳组大鼠DG区AS显著激活,胶质纤维酸性蛋白(GFAP)染色较深,细胞突起密集且细长。细胞面密度以及平均荧光强度均显著高于对照组(P<0.01);Western blot结果表明,相比于对照组,疲劳组大鼠海马组织CaMKⅡ蛋白磷酸化水平显著降低(P<0.01)。结论:运动疲劳导致了大鼠海马DG区PV-INs抑制,同时运动疲劳后AS的过度活化可能是造成海马DG区PV-INs抑制的重要因素,同时出现海马组织CaMKⅡ蛋白磷酸化水平的下降,进而损害了大鼠的空间识别记忆能力。
Objective:To investigate the neural regulatory mechanism of parvalbumin-positive interneurons(PV-INs)in the dentate gyrus(DG)involved in the impairment of spatial recognition memory by exercise-induced chronic fatigue.Methods:Male Sprague-Dawley(SD)rats were divided into control group and fatigue group by random number method.A three-level incremental load treadmill training program was selected to establish a chronic exhaustion exercise fatigue model.The spatial recognition memory ability of rats was tested by novel object recognition test.The activation levels and quantitative changes of astrocytes(AS)and PV-INs in the DG region was observed and quantified through immunofluorescence staining and immunohistochemical staining.The phosphorylation level of calcium/calmodulin-dependent protein kinase II(CaMKⅡ)in the hippocampus was detected by Western blot.Results:In the test of novel object recognition,the exploration time of novel object was reduced in the fatigue group,and the discrimination index was significantly lower than that in the control group(P<0.01).Immunohistochemical staining showed that PV-INs in the DG region of fatigue rats were lighter and fewer than those in the control group,the fibers were short and sparse,and the positive cell density and average optical density of cells were significantly lower than those in the control group(P<0.01).Immunofluorescence staining showed that AS was significantly activated,glial fibrillary acidic protein(GFAP)was stained deeply,and the cell processes were dense and elongated in the DG region of fatigue rats.The positive cell density and mean fluorescence intensity were significantly higher than those of the control group(P<0.01).The results of Western blot showed that the phosphorylation level of CaMKⅡprotein in the hippocampus of the fatigue group was significantly reduced than that of the control group(P<0.01).Conclusion:Exercise-induced chronic fatigue inhibited PV-INs in the rat hippocampal DG region.The excessive activation of AS following exercise fatigue may be a major contributor to this PV-INs suppression.Concurrently,reduced phosphorylation levels of CaMKⅡprotein were observed in hippocampal tissue.These alterations ultimately impaired spatial recognition memory in the rats.
作者
李鸿扬
林泐泉
苏畅
杨倩芸
曾少举
席超
孙丽娜
LI Hongyang;LIN Lequan;SU Chang;YANG Qianyun;ZENG Shaoju;XI Chao;SUN Lina(College of P.E and Sports,Beijing Normal University,Beijing 100875;Beijing Sanfan Middle School,Beijing 100088;College of Life Sciences,Beijing Normal University,Beijing 100875,China)
出处
《神经解剖学杂志》
北大核心
2025年第5期565-572,共8页
Chinese Journal of Neuroanatomy
基金
国家自然科学基金(32000835,32470493)
中国教育学会“第六批体育与卫生(国防教育)”专项课题(202300201312ZXB)。
关键词
运动疲劳
海马齿状回
空间识别记忆
PV阳性中间神经元
星形胶质细胞
CaMKⅡ
大鼠
exercise-induced chronic fatigue
dentate gyrus(DG)
spatial recognition and memory
parvalbumin-positive interneurons(PV-INs)
astrocytes(AS)
calcium/calmodulin-dependent protein kinase II(CaMKⅡ)
rat
