PATHOPHYSIOLOGY AND TREATMENT OF STRIATONIGRAL ISCHEMIC INJURY

对单侧可逆性大脑中脑缺血大鼠的纹状体黑质系统进行了行为学、磁共振成像和组织学研究，结果表明：(1)缺血15~120min的大鼠表现出全身注射多巴胺受体激动剂阿朴吗啡所致的扭体行为：(2)磁共振成像显示同侧纹状体和皮质较早出现T2高信号，且大小随缺血时间的延长而增大。Gd-DTPA增强磁共振成像显示短暂性脑缺血后血脑脊液屏障被破坏。(3)组织学上，大鼠同侧纹状体表现为亚部性脑缺血损伤。具有细胞类型特异性损伤的纹状体病变位于吻侧纹状体的背外侧部分。此外，黑质网状部外侧部分的纹状黑质传入纤维明显减少。缺血后同侧皮质和黑质的小胶质细胞被激活。(4)纹状体缺血区移植的免疫组织化学研究表明，移植的纹状体投射神经元改善了纹状体苍白质通路。

Behavioral, magnetic resonance imaging and histological studies were performed on the striatonigral system of rats with unilateral reversible middle cerebral occlusion, and following results were obtained.(1) The rats subjected to 15 to 120 minutes ischemia exhibited the ipsiversive rotational behavior elicited by systemic administration of dopamine receptor agonist apomorphine.(2) magnetic resonance imaging study showed that T2 high-signal-intensity aresa appeared earlier in the ipsilateral striatum and cortex and the size increased with the duration of ischemia. Disruption of the blood-cerebrospinal fluid barrier following transient ischemia was demonstrated by MR imaging using Gd-DTPA enhancement.(3) Histologically, the ipsilateral striatum of the rats showed a subdivisional ischemic injury. The striatal lesions having a cell type-specific injury were located in the dorsolateral portion of the rostral striatum. There was also a marked depletion of striatonigral afferents in the lateral portion of the substantia nigra pars reticulata. Activation of the microglia was noted in the ipsilateral cortex and the substantia nigra following ischemia.(4) Immunohistochemical study in the rat with striatal ischemic lesion followed by intrastriatal grafts derived from fetal striatal peimordia demonstrated that the striatopallidal pathway was reformend by striatal projection neurons of the transplants.