Dendrites and spines undergo dynamic changesin physiological conditions, such as learning and memory, and in pathological conditions, such as Alzheimer's diseaseand epilepsy. Long-term dendritic plasticity has also beenreported after ischemia/hypoxia, which might be compensatoryeffects of surviving neurons for the functional recoveryafter the insults. However, the dendritic changes shortly afterischemia, which might be associated with the pathogenesisof ischemic cell death, remain largely unknown. To reveal themorphological changes of ischemia-vulnerable neurons after ischemia, the present study investigated the alteration ofdendritic arborization of CA1 pyramidal neurons in rats aftertransient cerebral ischemia using intracellular staining techniquein vivo. The general appearance of dendritic arborizationof CA1 neurons within 48 h after ischemia was similar tothat of control neurons. However, a dramatic increase ofdendritic disorientation was observed after ischemia withmany basal dendrites coursed into the territory of apicaldendrites and apical dendrites branched into the region ofbasal dendrites. In addition, a significant increase of apicaldendritic length was found 24 h after ischemia. The increaseof dendritic length after ischemia was mainly due to thedendritic sprouting rather than the extension of individualdendrites, which mainly occurred in the middle segment ofthe apical dendrites. These results reveal a plasticity changein dendritic arborization of CA1 neurons shortly after cerebralischemia.

神经生长因子（NOF）可促进靶神经节神经突起生长晕的生长。本文应用sH-尿嘧啶核苷和3H一胸腺嘧啶核苷放射自显影术，进一步研究该作用与神经元合成RNA和DNA的关系。用新生大鼠颈上芍，按MaximoW双盖片法进行培养。培养物分NGF组（培养液内添加NGF粗制剂）和对照组（不用NGF）。NGF组培养物被3H一尿嘧啶核苷标记的神经元百分率及标记颗粒水平，均高于对照组，而且每当培养物神经突起生长晕生长速度即将出现高峰时，神经元3H一尿嘧啶核苷标记颗粒水平都明显地增高，说明NGF可促进颈上节神经元的RNA合成，i后者与神经突起的迅速生长有一定相互关系。在3H一胸腺嘧啶核苷标记培养物神经元的实验中，观察到NGF可促进培养第3天的颈上节少量的神经元合成DNA。

To investigate the synergistic effect of Schwann cells (SCs) and retinoic acid (RA) on differentiation andsynaptogenesis of neural stem cells (NSCs) derived from hippocampus of neonatal rats. Methods The classical methodfor 2