Di Chiara G, Morelli M, Porceddu M L, Mulas M, Del Fiacco M
Brain Res. 1980 May 5;189(1):193-208. doi: 10.1016/0006-8993(80)90017-7.
Locally applied kainic acid was used in order to destroy pallidal perikarya without damaging axons en passage, in an effort to clarify the role of the globus pallidus as a source of nigral GABAergic terminals. Rats were microinjected unilaterally with kainic acid in the globus pallidus, head, body and tail of the caudate and were sacrificed 7 days later. The forebrain of each rat was examined histologically in order to establish the extent of the lesion and nigral glutamate decarboxylase (GAD) was assayed as a marker of GABAergic terminals. Kainic acid produced in the globus pallidus loss of neuronal perikarya and reactive gliosis. Large multipolar neurons of the globus pallidus were characteristically absent on the lesioned-side. Lesions of the pallidum resulted in a non-significant (5.5%) reduction of nigral GAD. Kainate lesions restricted to the head of the caudate resulted in a significant (19%) drop of nigral GAD, while lesions of the caudate body provided the largest reductions of nigral GAD (53%). Lesions of the caudate tail were without effect. The results indicate that nigral GAD arises mostly from the body and, in part, also from the head of the caudate but not from the globus pallidus or from the tail of the caudate.
为了在不损伤过路轴突的情况下破坏苍白球神经元胞体，以阐明苍白球作为黑质γ-氨基丁酸（GABA）能终末来源的作用，采用了局部应用海人酸的方法。将大鼠单侧苍白球、尾状核头部、体部和尾部微量注射海人酸，7天后处死。对每只大鼠的前脑进行组织学检查以确定损伤范围，并检测黑质谷氨酸脱羧酶（GAD）作为GABA能终末的标志物。海人酸导致苍白球神经元胞体丧失和反应性胶质增生。损伤侧特征性地缺失了苍白球的大型多极神经元。苍白球损伤导致黑质GAD无显著降低（5.5%）。局限于尾状核头部的海人酸损伤导致黑质GAD显著下降（19%），而尾状核体部损伤导致黑质GAD下降幅度最大（53%）。尾状核尾部损伤无影响。结果表明，黑质GAD主要来自尾状核体部，部分也来自尾状核头部，而非来自苍白球或尾状核尾部。
