大鼠Meynert基底核TrkA和ChAT的表达

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

THE EXPRESSION OF TrkA AND ChAT IN THE BASAL NUCLEUS OF MEYNERT IN RATS OF DIFFERENT AGE

The distribution of TrkA and the postnatal development(PD) of TrkA and ChAT immunoreactive( IR) neurons and the relation between them in the basal nucleus of Meynert of rats were studied with immunohistochemical method. The number, mean profile areas and grey degree of TrkA IR and ChAT IR neurons were examined with image analyser. The data revealed that TrkA IR neurons were localized in the basal forebrain of rats. TrkA immunostaining was present at PD1, but ChAT was not. ChAT immunostaining was present at PD5. Most densely stained TrkA and ChAT neuronal bodies and fibers were present at PD20, the mean grey degrees of TrkA IR and ChAT IR neuronal profiles reached its peak. Both TrkA and ChAT neurons began to cline at PD30 and maintained a relatively higher level in the adult. However, during aging both TrkA and ChAT IR neurons atrophy and became smaller than that in the adult. The number of TrkA IR and ChAT IR neurons were decreased by 41.38% and 51.61%; the mean profile areas decreased by 15.7% and 12.8%; and the mean grey degrees by 29.9% and 9.9%, respectively. The mean profile areas of TrkA IR and ChAT IR neurons from PD5 to aged rats were positively correlated. The results indicated that the expression of TrkA was earlier than ChAT. The expression of TrkA and ChAT followed a very similar temporal pattern in the basal nucleus of Meynert from PD5 to aged rats, suggesting that TrkA might participate the regulation of ChAT IR neuronal development, differentiation, maturation, and ageing. The down regulation of TrkA and ChAT of aged rats is associated with neuronal atrophy and loss and may contribute to the pronounced vulnerability of these neurons to degeneration in aging animals and Alzheimer's disease.