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目的 了解大鼠基底前脑斜角带核水平支神经元内酪氨酸激酶 A(tyrosine kinase A,Trk A)、胆碱乙酰化转移酶 (choline acetyltransferase,Ch AT)样阳性神经元的生后发育规律及两者的相互关系。 方法 用免疫组织化学方法结合图像分析仪检测大鼠基底前脑斜角带核水平支 Trk A、Ch AT样阳性神经元的数量、面积和灰度值。 结果 Trk A、Ch AT分布于基底前脑神经元。生后 1d可见 Trk A表达 ,但生后 5 d才出现 Ch AT表达。生后 2 0 dTrk A、Ch AT表达至高峰 ;生后 30 d下调 ,成年时维持相对较高水平。老年鼠 Trk A、Ch AT样阳性神经元出现萎缩、数量也分别减少 39.7%、33.3% ;胞体平均面积分别减少 15 .7%、12 .8% ;平均灰度值分别减少 2 9.9%、9.9%。同时 ,不同年龄大鼠 Trk A、Ch AT样阳性神经元截面积和灰度呈弱正相关 ,数量呈正相关。 结论 大鼠基底前脑斜角带核水平支神经元 Trk A表达早于 Ch AT表达。从生后 5 d起 ,Trk A、Ch AT表达有相似的时间模式。Trk A可能参与斜角带核胆碱能神经元的发育、分化、成熟和老化。老年鼠 Trk A、Ch AT表达下调可能是老年动物和阿尔茨海默病人基底前脑胆碱能神经元变性的易感性增加的原因之一。
Objective To investigate the effect of tyrosine kinase A (Trk A) and choline acetyltransferase (ChAT) -like neurons in the basal forebrain of the basal forebrain, Developmental rules and the relationship between the two. Methods Immunohistochemistry and image analyzer were used to detect the number, area and gray value of Trk A, Ch AT-like neurons in the basal forebrain oblique basal ganglia. Results Trk A and Ch AT were distributed in basal forebrain neurons. One week after birth, Trk A expression was seen, but Ch AT expression appeared only 5 days after birth. The expression of Trk A and ChAT was peaked at 20 days after birth, and down-regulated at 30 days after birth, and maintained a relatively high level in adulthood. The number of AT-like neurons of Trk A and Ch-like neurons in aged mice decreased by 39.7% and 33.3%, respectively. The average area of the somatic cells decreased by 15.7% and 12.8% respectively, while the average gray value decreased by 2.9% and 9.9% respectively %. At the same time, the cross-sectional area and gray level of Trk A and Ch AT-like neurons in different age groups showed a weak positive correlation with a positive correlation. Conclusion The expression of Trk A in nucleus propria of basal forebrain oblique nucleus is earlier than that of Ch AT. From the 5th day after birth, Trk A and Ch AT expressed similar time pattern. Trk A may be involved in the development, differentiation, maturation, and aging of the nucleus-dorsal cholinergic neurons. The downregulation of Trk A and Ch AT expression in aged mice may be one of the reasons for the increased susceptibility of basal forebrain cholinergic neurons in aged animals and Alzheimer’s patients.