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本实验用免疫组织化学方法研究了 Trk A在大鼠 Meynert基底核的分布及 Trk A、Ch AT免疫反应神经元的生后发育及两者表达的相互关系。用图像分析仪检测 Meynert基底核 Trk A-、Ch AT-IR神经元的数量、截面积和灰度值。结果表明 : Tr-k A、Ch AT分布于 Meynert基底核神经元。生后 1d可见 Trk A表达 ,但未见 Ch AT表达 ;生后 5 d方出现 Ch AT表达 ;生后 2 0 dTrk A、Ch AT表达达高峰 ;生后 3 0 d下降 ,到成年时维持相对较高水平。老龄鼠 Trk A-、Ch AT-IR神经元萎缩 ,数量分别减少 41.3 8%和 5 1.61% ,胞体平均截面积分别减少 3 9.4%和 3 0 .4% ,平均灰度值分别减少 11.8%和 9.9%。大鼠 Trk A-、Ch AT-IR神经元截面积呈正相关。大鼠 Meynert基底核神经元 Trk A表达早于 Ch AT表达 ,从生后 5 d开始 ,Trk A、Ch AT表达有相似的时间模式。 Trk A可能参与 Meynert基底核胆碱能神经元的发育、分化、成熟和老化。老龄鼠 Trk A、Ch AT表达下降可能是老年动物和老年性痴呆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
In this study, immunohistochemistry was used to study the distribution of Trk A in the basal ganglia of Meynert and the relationship between the expression of Trk A and ChAT immunoreactive neurons and their postnatal development. The number, cross-sectional area and gray value of Trk A- and Ch -AT-IR neurons in Meynert’s nucleus were detected by image analyzer. The results showed that Tr-k A and Ch AT were distributed in neurons of Meynert basal ganglia. The expression of Trk A was seen on the 1st day after birth, but not on the expression of Ch AT at 5 days after birth. The expression of ChAT was observed on the 5th day after birth, and reached the peak on the 20th day after birth. The expression of ChAT was decreased on the 30th day after birth, Higher level. The number of apoptotic Trk A- and Ch -AT-IR neurons in old rats decreased by 41.3 8% and 5 1.61%, respectively. The average cross-sectional area decreased by 34.4% and 34.4%, and the average gray value decreased by 11.8% and 9.9%. The cross-sectional area of Trk A- and Ch -AT-IR neurons in rats was positively correlated. The expression of Trk A in neurons of Meynert basal ganglia in rats was earlier than that in Ch AT, and the expression patterns of Trk A and Ch AT were similar in time pattern from the 5th day after birth. Trk A may be involved in the development, differentiation, maturation and aging of basal nucleolar choroidal neurons in Meynert. Decreased expression of Trk A and Ch AT in aged rats may be one of the reasons for the increased susceptibility of cholinergic neurons degeneration in basal forebrain in aged animals and senile dementia patients