Krammer E B
Brain Res. 1980 Aug 25;196(1):209-21. doi: 10.1016/0006-8993(80)90727-1.
Damage of striatal neurons by kainic acid (KA) induces an anterograde and transsynaptic degeneration 'en cascade' in the globus pallidus (GP) and substantia nigra (SN). By causing only degeneration of projections arising from KA-sensitive striatal neurons while sparing the connections of KA-resistant striatal neurons, the lesion-induced alterations of the basal ganglia show a characteristic pattern which bears a close resemblance with the neuropathological changes occurring in Huntington's disease: (1) severe degeneration of small and medium-sized striatal neurons, of pallidal neurons and the neurons of the pars reticulata of the SN, and (2) sparing of large striatal neurons, 'peripallidal' (nucleus basalis) neurons and neurons of the pars compacta of the SN. The probable interconnections of both the degenerated and the spared neuronal groups are discussed with respect to the present concept of the neuronal organization and biochemical neuroanatomy of the basal ganglia.
kainic酸(KA)对纹状体神经元的损伤会在苍白球(GP)和黑质(SN)中引发顺行性和跨突触的“级联”变性。通过仅导致KA敏感的纹状体神经元发出的投射发生变性,同时保留KA抗性纹状体神经元的连接,损伤诱导的基底神经节改变呈现出一种特征性模式,与亨廷顿病中发生的神经病理变化极为相似:(1)中小型纹状体神经元、苍白球神经元和黑质网状部神经元严重变性,(2)大型纹状体神经元、“苍白球周围”(基底核)神经元和黑质致密部神经元未受影响。结合基底神经节神经元组织和生化神经解剖学的当前概念,讨论了变性和未受影响神经元群可能的相互连接。