Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.
Proc Natl Acad Sci U S A. 2009 Nov 10;106(45):18890-6. doi: 10.1073/pnas.0910659106. Epub 2009 Nov 3.
Neural activity can induce persistent strengthening or weakening of synapses, known as long-term potentiation (LTP) or long-term depression (LTD), respectively. As potential cellular mechanisms underlying learning and memory, LTP and LTD are generally regarded as synapse-specific "imprints" of activity, although there is evidence in vitro that LTP/LTD may spread to adjacent synapses. Here, we report that LTP and LTD induced in vivo at retinotectal synapses of Xenopus tadpoles undergo rapid long-range retrograde spread from the optic tectum to the retina, resulting in potentiation and depression of bipolar cell synapses on the dendrites of retinal ganglion cells, respectively. The retrograde spread of LTP and LTD required retrograde signaling initiated by brain-derived neurotrophic factor and nitric oxide in the tectum, respectively. Such bidirectional adjustment of the strength of input synapses in accordance to that of output synapses may serve to coordinate developmental refinement and learning functions of neural circuits.
神经活动可以诱导突触的持久增强或减弱，分别称为长时程增强（LTP）或长时程抑制（LTD）。作为学习和记忆的潜在细胞机制，LTP 和 LTD 通常被视为活动的突触特异性“印记”，尽管有体外证据表明 LTP/LTD 可能会扩散到相邻的突触。在这里，我们报告说，在非洲爪蟾蝌蚪的视网膜-顶盖突触中诱导的 LTP 和 LTD 会从顶盖快速逆行传播到视网膜，导致双极细胞突触在视网膜神经节细胞的树突上分别被增强和抑制。LTP 和 LTD 的逆行传播分别需要顶盖中脑源性神经营养因子和一氧化氮引发的逆行信号。这种根据输出突触的强度来调节输入突触强度的双向调整可能有助于协调神经回路的发育细化和学习功能。
