帕金森病小鼠黑质calbindin-D28k mRNA的表达

目的　研究钙结合素D28k（CaBP）在帕金森病（PD）发病机制中的作用.方法　给C57BL小鼠ip 1-甲基-4-苯基-1，2，3，6-四氢吡啶 (MPTP)，30 mg*kg-1MPTP每24 h注射1次，连续应用3 d以建立PD鼠模型.用原位杂交法检测CaBP mRNA在PD鼠和对照鼠黑质神经元中的表达变化.结果　CaBP mRNA阳性神经元主要分布于黑质致密部（SNC）.在MPTP处理鼠的SNC神经元，CaBP mRNA的表达水平明显降低.模型鼠和对照鼠的SNC中CaBP mRNA阳性神经元的数量有差异(144±15) vs (88±10)，(P<0.05).与对照相比，MPTP处理组小鼠SNC中表达CaBP mRNA神经元的杂交信号强度也有降低.结论　CaBP可能通过对黑质多巴胺能神经元的保护作用来抵御PD的发生.

Calbindin-D28k mRNA expression in substantia nigra in mice Parkinson's disease

AIM　To investigate the possible role of calbindin-D28k（CaBP）in the pathogenesis of Parkinson's disease (PD).METHODS　C57BL mice were intraperitoneally treated with 1-methyl-4-phenyl-1,2,3,6-terahydropyridine (MPTP).30 mg*kg-1 MPTP was injected every 24 h for 3 consecutive days to establish PD mice models.In situ hybridization was then performed to detect the expression changes of CaBP mRNA in the neurons of the substantia nigra in the MPTP-treated and control mice.RESULTS　Neurons expressing CaBP mRNA were preferentially localized in the substantia nigra pars compacta (SNC).In the mice treated with MPTP, there was a significant decrease of CaBP mRNA levels in the neurons of SNC.The numbers of CaBP-positive neurons in the SNC in controls and MPTP-treated mice were (144±15.1) and (88±10) respectively (P<0.05).Compared with the controls, the hybridization signal densities of CaBP mRNA-expressing neurons in pathological models also decreased.CONCLUSION　CaBP may provide some protection to SNC dopaminergic neurons against the pathological process responsible for PD.