不同年龄大鼠斜角带核水平支神经元内TrkA和ChAT的表达——免疫组织化学研究

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，ＴｒｋＡ）、胆碱乙酰化转移酶（ｃｈｏｌｉｎｅ ａｃｅｔｙｌｔｒａｎｓｆｅｒａｓｅ，ＣｈＡＴ）样阳性神经元的生后发育规律及两乾的相互关系。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ＴｒｋＡ、ＣｈＡＴ样阳性神经元的数量、面积和灰度值。结果 ＴｒｋＡ、ＣｈＡＴ分布于基底前脑神经元。生后１ｄ可见ＴｒｋＡ表达，但生后５ｄ才出现ＣｈＡＴ表达。生后２０ｄＴｒｋＡ、ＣｈＡＴ表达至高峰；生后３０ｄ下调，成年时维持相对较高水平。老年鼠ＴｒｋＡ、ＣｈＡＴ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２９．９％、９．９％。同时，不同年龄大鼠Ｔ

THE EXPRESSION OF TrkA AND ChAT IN NEURONS OF THE HORIZONTAL LIMB OF DIAGONAL BAND OF DIFFERENTLY AGED RATS -- AN IMMUNOHISTOCHEMICAL STUDY

Objective To investigate the postnatal developmental rule of TrkA and ChAT\|immunoreactive(ChAT\|ir) neurons and the relationship between TrkA and ChAT\|ir neurons in the horizontal limb of diagonal band(HDB) of rats. Methods Immunohistochemistry technique combined with image analyser were used. Results TrkA and ChAT\|ir neurons localized in the neurons of basal forebrain of rats. TrkA immunostaining was present at postnatal day 1(PD1), but ChAT immunostaining was present at PD5 Most densely stained TrkA and ChAT neuronal bodies and fibers were present at PD20, while the mean grey degrees of TrkA and ChAT\|ir neurons reached to the peak. Both TrkA and ChAT began to decline at PD30 and maintain a relatively higher level in the adult. However, during aging both TrkA and ChAT\|ir neurons atrophied and became smaller than that of adult. The number of TrkA and ChAT\|ir neurons decreased 39 8% and 33 3%;the mean areas 15 7% and 12 8%; the mean grey degree values were 29 9% and 9 9%, respectively. The mean areas, grey degrees and numbers of TrkA and ChAT\|ir neurons from PD5 to aged rats had positive correlation. Conclusion The results indicate that the expression of TrkA was earlier than ChAT. The expression of TrkA and ChAT followed a very similar temporal pattern in HDB from PD5 to aged rats, suggesting that TrkA may participate in the regulation of ChAT\|ir neuronal development, differentiation, maturation and aging. 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 disease.