Prenatally compromised neurons respond to brain-derived neurotrophic factor treatment in vitro
Prenatally compromised neurons respond to brain-derived neurotrophic factor treatment in vitro
复制标题
DOI：
10.1097/01.wnr.0000233104.51149.9c
复制
发表时间：
2006-09-18
期刊：
影响因子：
1.7
通讯作者：
Rees, Sandra M.
中科院分区：
文献类型：
--
作者：
Briscoe, Todd A.;Tolcos, Mary;Rees, Sandra M.
产前缺氧影响神经元存活和突起生长。影响神经生长的脑源性神经营养因子在这些条件下减少。我们测试了添加脑源性神经营养因子是否能增强从妊娠30-52天（类似于67天）的慢性胎盘功能不全的豚鼠胎儿（n=7）培养的神经元的生长。从嗅球、海马和小脑制备培养物。与对照组（n=7）相比，慢性胎盘功能不全导致嗅球培养物中神经突总长度减少。脑源性神经营养因子治疗5天增加了总嗅神经突长度和体大小和数量的初级神经突在所有文化的控制和妥协的动物。因此，脑源性神经营养因子可以影响受损的胎儿神经元的生长，支持其在慢性胎盘功能不全后的治疗用途。
Prenatal hypoxia affects neuronal survival and process outgrowth. Brain-derived neurotrophic factor, which influences neural growth, is decreased in these conditions. We tested whether addition of brain-derived neurotrophic factor enhances growth of neurons cultured from guinea pig fetuses (n=7) compromised by chronic placental insufficiency from 30-52 days gestation (term similar to 67 days). Cultures were prepared from the olfactory bulb, hippocampus and cerebellum. Compared with controls (n=7), chronic placental insufficiency resulted in reduced total neurite length in olfactory bulb cultures. Brain-derived neurotrophic factor treatment for 5 days increased the total olfactory neurite length and somal size and number of primary neurites in all cultures from both control and compromised animals. Thus, brain-derived neurotrophic factor can influence the growth of compromised fetal neurons supporting its therapeutic use following chronic placental insufficiency.