摘要
研究成年大鼠脑室下区 (SVZ)神经前体细胞 (neural precursors)在黑质 -纹状体通路损伤后的反应 ,本研究用 6-羟多巴胺单侧纹状体注射以损毁黑质 -纹状体通路 ,损毁 10 d后腹腔注射 Brd U ,连续 4d,每日两次 ;在 SVZ、纹状体和黑质部位用免疫组化方法检测 Brd U、nestin以及 GFAP阳性细胞。结果显示 :(1) 6-羟多巴胺损毁黑质 -纹状体通路后 ,伤侧 SVZ的 Brd U阳性细胞数明显增多 ,并成簇分布 ;nestin和 GFAP阳性细胞数也增多 ,但以 GF AP阳性细胞增多明显 ;(2 )伤侧纹状体可见大量 Br-d U、GFAP以及少量 nestin阳性细胞分布 ,而健侧只有少量 GFAP阳性细胞 ;(3 )伤侧可见 Brd U阳性细胞在 SVZ和纹状体之间呈条带样分布 ;(4 )伤侧黑质除酪氨酸羟化酶阳性神经元减少外 ,未见 Brd U、GFAP和 nestin阳性细胞表达。上述结果表明 ,6-羟多巴胺损毁黑质 -纹状体通路后 ,SVZ神经前体细胞活动增强 ,有向纹状体迁移的趋势。
To study the responsibility of neural precursors in the subventricular zone in adult rat after a unilateral lesion in the nigrostriatal pathway, the 6-hydroxydopamine(6-OHDA) was unilaterally injected into the striatum in adult rat. 10 days later, bromodeoxyuridine (BrdU) was injected (i.p.) twice a day for 4 days in those rats. The brain sections were immunohistochemically stained to detect BrdU-, glial fibrillary acidic protein (GFAP)-, nestin- and tyrosine hydroxylase (TH)- immunoreactive cells in the subventicular zone, the striatum and the substantia nigra. The results showed that the BrdU- positive cells increased significantly in the SVZ ipsilateral to the striatal injection. Also, the number of GFAP-, nestin-positive cells were increased specially in the same side of SVZ zone. A large number of BrdU-, GFAP- and nestin-labelled cells were seen in the injected side of the striatum, compared with only a few of GFAP positive cells in contralateral side. Some BrdU-positive cells were showed to have tendency of migration from the SVZ to lesioned striatum. Neither BrdU-labeled cells nor GFAP- and nestin-labeled cells were found on both sides of substantia nigra after the lesion, although the TH-positive cells were decreased dramatically. The results suggest that the neural precursors in the SVZ can be increased and migrated after a lesion in the nigrostriatal pathway in the adult rat.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2004年第4期383-388,共6页
Chinese Journal of Neuroanatomy
基金
国家重点基础研究计划 (脑基础及脑重大疾病的基础研究 ) (G19990 5 40 0 8)
北京市科委自然科学基金 (95 5 5 10 12 0 0 )资助项目