Dept. of Brain & Cognitive Sciences, College of Natural Sciences, Seoul National University, Gwanak-gu, Seoul 151-746, South Korea.
Neuropharmacology. 2013 Nov;74:86-95. doi: 10.1016/j.neuropharm.2013.01.011. Epub 2013 Jan 25.
Phosphodiesterases (PDEs) degrade cyclic nucleotides, signalling molecules that play important roles in synaptic plasticity and memory. Inhibition of PDEs may therefore enhance synaptic plasticity and memory as a result of elevated levels of these signalling molecules, and this has led to interest in PDE inhibitors as cognitive enhancers. The development of new mouse models in which PDE subtypes have been selectively knocked out and increasing selectivity of PDE antagonists means that this field is currently expanding. Roles for PDE2, 4, 5 and 9 in synaptic plasticity have so far been demonstrated and we review these studies here in the context of cyclic nucleotide signalling more generally. The role of other PDE families in synaptic plasticity has not yet been investigated, and this area promises to advance our understanding of cyclic nucleotide signalling in synaptic plasticity in the future. This article is part of the Special Issue entitled 'Glutamate Receptor-Dependent Synaptic Plasticity'.
磷酸二酯酶(PDEs)可降解环核苷酸,作为信号分子在突触可塑性和记忆中发挥重要作用。因此,抑制 PDE 可能会提高这些信号分子的水平,从而增强突触可塑性和记忆,这使得 PDE 抑制剂作为认知增强剂引起了人们的兴趣。选择性敲除 PDE 亚型的新型小鼠模型的开发以及 PDE 拮抗剂选择性的提高意味着该领域目前正在不断扩展。目前已经证明了 PDE2、4、5 和 9 在突触可塑性中的作用,我们在此综述了这些研究,同时还综述了更广泛的环核苷酸信号转导。其他 PDE 家族在突触可塑性中的作用尚未得到研究,这一领域有望增进我们对突触可塑性中环核苷酸信号转导的理解。本文是主题为“谷氨酸受体依赖性突触可塑性”的特刊的一部分。