A trial of neurofunctional recovery after brain damage by neurotrophic factor and neural transpolant.

皮质受损导致同侧丘脑进行性变性。纹状体的缺血性损伤导致同侧黑质的远端病变。神经营养因子或神经移植可以改善这些退行性病变。我们分别研究了皮质损伤或纹状体损伤后丘脑或黑质的代谢、功能和形态的变化。我们还研究了神经营养因子之一的碱性成纤维细胞生长因子(b-FGF)对丘脑神经元的影响。单单位记录显示皮质消融后丘脑神经元的突触传递受到抑制。B-成纤维细胞生长因子可改善丘脑退行性变，但不能改善丘脑神经元的突触传递，皮质梗塞也可引起丘脑变性。脱氧葡萄糖放射自显影显示大鼠急性期(皮质梗死后3天、7天)低代谢后的慢性期(皮质梗塞后1个月)丘脑出现异常的高代谢。免疫组织化学研究表明，丘脑的这种高代谢是由小胶质细胞反应引起的。纹状体梗塞导致大鼠黑质跨神经元变性。纹状体梗塞后7天，我们还观察到同侧黑质的葡萄糖高代谢。然而，单单位记录显示纹状体梗死后7天和14天黑质神经元没有过度兴奋。

Damage of cortex results in progressive degeneration in the ipsilateral thalamus. Ischemic damage to the striatum leads to remote pathological changes in the ipsilateral substantia nigra. It has been expected that these degenerations are improved by neurotrophic factors or neural transplant. We studied the metabolic, functional and morphological changes in the thalamus or the substantia nigra following cortical damage or striatal damage, respectively. We also studied the effects of basic fibroblast growth factor (b-FGF), one of neurotrophic factors, on the thalamic neurons.Cortical ablation resulted in degeneration of the thalamus in rats. Single unit recording revealed depression of synaptic transmission in the thalamic neurons after cortical ablation. The b-FGF ameliorated the thalamic degeneraiton, however, the synaptic transmission of the thalamic neurons was not improved by the b-FGF.Cortical infarction also caused degeneration of the thalamus in rats. Deoxyglucose autoradiographic study showed abnormal hypermetabolism of the thalamus in the chronic stage (1 month after cortical infarction) following hypometabolism in the acute stage (3,7 days after cortical infarction) in rats. Immunohistochemical study suggested that this hypermetabolism of the thalamus was attributed to the microglial reaction. Striatal infarction resulted in transneuronal degeneration of the substantia nigra in rats. We also observed glucose hypermetabolism in the ipsilateral substantia nigra 7 days after striatal infarction. However, Single unit recording showed no hyper-exciting substantia nigra neurons 7 and 14 days after striatal infarction.