Boulanger L M, Poo M M
Department of Biology, University of California at San Diego, La Jolla 92093-0357, USA.
Nat Neurosci. 1999 Apr;2(4):346-51. doi: 10.1038/7258.
Neurotrophins have been proposed to participate in activity-dependent modifications of neuronal connectivity and synaptic efficacy. Preferential strengthening of active inputs requires restriction of putative neurotrophin-mediated synaptic potentiation to active synapses. Here we report that potentiation of synaptic efficacy by brain-derived neurotrophic factor (BDNF) is greatly facilitated by presynaptic depolarization at developing neuromuscular synapses. Brief depolarization in the presence of low-level BDNF results in a marked potentiation of both evoked and spontaneous synaptic transmission, whereas exposure to either BDNF or depolarization alone is without effect. This potentiation depends on the relative timing of depolarization and reflects an enhancement of transmitter secretion from the presynaptic neuron. Thus synapses made by active inputs may be selectively strengthened by secreted neurotrophins as part of activity-dependent refinement of developing connections or of mature synapses.
神经营养因子被认为参与了神经元连接和突触效能的活动依赖性修饰。活性输入的优先强化需要将假定的神经营养因子介导的突触增强限制在活性突触上。在这里，我们报告在发育中的神经肌肉突触处，脑源性神经营养因子（BDNF）介导的突触效能增强在很大程度上受到突触前去极化的促进。在低水平BDNF存在下的短暂去极化会导致诱发和自发突触传递的显著增强，而单独暴露于BDNF或去极化则没有效果。这种增强取决于去极化的相对时间，并反映了突触前神经元递质分泌的增强。因此，作为发育中连接或成熟突触的活动依赖性精细化的一部分，由活性输入形成的突触可能会被分泌的神经营养因子选择性地增强。
