Division of Pharmacology and Neurobiology, Biozentrum, University of Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
Cerebellum. 2010 Sep;9(3):284-90. doi: 10.1007/s12311-010-0174-9.
In the last decade, several experimental studies have demonstrated that particular patterns of synaptic activity can induce postsynaptic parallel fiber (PF) long-term potentiation (LTP). This form of plasticity can reverse postsynaptic PF long-term depression (LTD), which has been traditionally considered as the principal form of plasticity underlying cerebellar learning. Postsynaptic PF-LTP requires a transient increase in intracellular Ca(2+) concentration and, in contrast to PF-LTD, is induced without concomitant climbing fiber (CF) activation. Thus, it has been postulated that the polarity of long-term synaptic plasticity is determined by the amplitude of the Ca(2+) transient during the induction protocol, with PF-LTP induced by smaller Ca(2+) signals without concomitant CF activation. However, this hypothesis is contradicted by recent studies. A quantitative analysis of Ca(2+) signals associated with induction of PF-LTP indicates that the bidirectional induction of long-term plasticity is regulated by more complex mechanisms. Here we review the state-of-the-art of research on postsynaptic PF-LTP and PF-LTD and discuss the principal open questions on this topic.
在过去的十年中,有几项实验研究表明,特定模式的突触活动可以诱导突触后平行纤维(PF)长时程增强(LTP)。这种形式的可塑性可以逆转传统上被认为是小脑学习基础的突触后 PF 长时程抑制(LTD)。突触后 PF-LTP 需要细胞内 Ca(2+)浓度的短暂增加,与 PF-LTD 不同,它是在没有伴随的 climbing fiber (CF) 激活的情况下诱导的。因此,有人提出,长期突触可塑性的极性取决于诱导过程中 Ca(2+)瞬变的幅度,较小的 Ca(2+)信号而没有伴随的 CF 激活诱导 PF-LTP。然而,最近的研究反驳了这一假设。对与诱导 PF-LTP 相关的 Ca(2+)信号的定量分析表明,长期可塑性的双向诱导是由更复杂的机制调节的。本文综述了突触后 PF-LTP 和 PF-LTD 的研究现状,并讨论了该领域的主要开放性问题。