Feng L, Wang C Y, Jiang H, Oho C, Mizuno K, Dugich-Djordjevic M, Lu B
Laboratory of Developmental Neurobiology, NICHD, NIH, Bethesda, MD 20892-4480, USA.
Brain Res Mol Brain Res. 1999 Mar 20;66(1-2):62-70. doi: 10.1016/s0169-328x(99)00015-7.
Previous studies have shown that brain derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) can enhance the survival of dopaminergic neurons in the ventral mesencephalon (VM). Here we compared several non-survival functions of the two factors in VM neurons in culture. We found that both BDNF and GDNF elicited an increase in the depolarization-induced release of dopamine, but had no effect on GABA release, in the VM cultures. BDNF, but not GDNF, significantly enhanced the expression of the calcium binding protein calbindin and synaptic protein SNAP25. In contrast, treatment of the cultures with GDNF, but not BDNF, elicited a marked fasciculation of the processes of the VM neurons. Thus, although both act on VM neurons, BDNF and GDNF have distinct functions.
先前的研究表明,脑源性神经营养因子(BDNF)和胶质细胞系源性神经营养因子(GDNF)可增强中脑腹侧(VM)多巴胺能神经元的存活。在此,我们比较了这两种因子在培养的VM神经元中的几种非存活功能。我们发现,在VM培养物中,BDNF和GDNF均可引起去极化诱导的多巴胺释放增加,但对GABA释放无影响。BDNF可显著增强钙结合蛋白钙结合蛋白和突触蛋白SNAP25的表达,而GDNF则无此作用。相反,用GDNF而非BDNF处理培养物可引起VM神经元突起的明显成束。因此,尽管BDNF和GDNF均作用于VM神经元,但它们具有不同的功能。