Wang X H, Poo M M
Department of Biology, University of California at San Diego, La Jolla 92093-0357, USA.
Neuron. 1997 Oct;19(4):825-35. doi: 10.1016/s0896-6273(00)80964-2.
The hypothesis that synaptic functions can be regulated by neurotrophins secreted from the postsynaptic cell was examined in Xenopus nerve-muscle cultures. Neuromuscular synapses formed on myocytes overexpressing neurotrophin-4 (M+ synapses) exhibited a higher level of spontaneous synaptic activity and enhanced evoked synaptic transmission as compared to those formed on normal control myocytes (M- synapses). The NT-4 effects involve a potentiation of presynaptic transmitter secretion as well as a lengthening of the mean burst duration of postsynaptic low conductance acetylcholine channels. Repetitive stimulation of either the presynaptic neuron or the postsynaptic myocyte led to a potentiation of synaptic transmission at M+ synapses. All potentiation effects of NT-4 overexpression were abolished by the extracellular presence of TrkB-IgG but not by the presence of TrkA-IgG, indicating that postsynaptic secretion of NT-4 was responsible for the synaptic modification.
在非洲爪蟾神经肌肉培养物中，研究了突触后细胞分泌的神经营养因子可调节突触功能这一假说。与在正常对照肌细胞（M-突触）上形成的神经肌肉突触相比，在过表达神经营养因子-4的肌细胞上形成的神经肌肉突触（M+突触）表现出更高水平的自发突触活动，并增强了诱发突触传递。神经营养因子-4的作用包括增强突触前递质分泌以及延长突触后低电导乙酰胆碱通道的平均爆发持续时间。对突触前神经元或突触后肌细胞的重复刺激导致M+突触处的突触传递增强。细胞外存在TrkB-IgG可消除神经营养因子-4过表达的所有增强作用，但TrkA-IgG的存在则不能消除，这表明突触后分泌的神经营养因子-4是突触修饰的原因。
