Okada Daisuke, Ozawa Fumiko, Inokuchi Kaoru
Mitsubishi Kagaku Institute of Life Sciences (MITILS), 11 Minamiooya, Machida, Tokyo 194-8511, Japan.
Science. 2009 May 15;324(5929):904-9. doi: 10.1126/science.1171498.
Late-phase synaptic plasticity depends on the synthesis of new proteins that must function only in the activated synapses. The synaptic tag hypothesis requires input-specific functioning of these proteins after undirected transport. Confirmation of this hypothesis requires specification of a biochemical tagging activity and an example protein that behaves as the hypothesis predicts. We found that in rat neurons, soma-derived Vesl-1S (Homer-1a) protein, a late-phase plasticity-related synaptic protein, prevailed in every dendrite and did not enter spines. N-methyl-d-aspartate receptor activation triggered input-specific spine entry of Vesl-1S proteins, which met many criteria for synaptic tagging. These results suggest that Vesl-1S supports the hypothesis and that the activity-dependent regulation of spine entry functions as a synaptic tag.
晚期突触可塑性依赖于新蛋白质的合成，这些新蛋白质必须仅在被激活的突触中发挥作用。突触标记假说要求这些蛋白质在无定向运输后进行输入特异性功能。对这一假说的证实需要确定一种生化标记活性以及一个表现如假说所预测的示例蛋白质。我们发现，在大鼠神经元中，源自胞体的Vesl-1S（Homer-1a）蛋白，一种与晚期可塑性相关的突触蛋白，在每个树突中都占主导地位，且不进入棘突。N-甲基-D-天冬氨酸受体激活触发了Vesl-1S蛋白的输入特异性棘突进入，这满足了突触标记的许多标准。这些结果表明，Vesl-1S支持这一假说，且棘突进入的活性依赖性调节起到了突触标记的作用。
