Pasinelli P, Ramakers G M, Urban I J, Hens J J, Oestreicher A B, de Graan P N, Gispen W H
Department of Medical Pharmacology, Rudolf Magnus Institute for Neuroscience, Utrecht University, The Netherlands.
Behav Brain Res. 1995 Jan 23;66(1-2):53-9. doi: 10.1016/0166-4328(94)00124-x.
Long-term potentiation (LTP) is a well known experimental model for studying the activity-dependent enhancement of synaptic plasticity, and because of its long duration and its associative properties, it has been proposed as a system to investigate the molecular mechanisms of memory formation. At present, there are several lines of evidence that indicate that pre- and postsynaptic kinases and their specific substrates are involved in molecular mechanisms underlying LTP. Many studies focus on the involvement of protein kinase C (PKC). One way to investigate the role of PKC in long-term potentiation is to determine the degree of phosphorylation of its substrates after in situ phosphorylation in hippocampal slices. Two possible targets are the presynaptic membrane-associated protein B-50 (a.k.a. GAP 43, neuromodulin and F1), which has been implicated in different forms of synaptical plasticity in the brain such as neurite outgrowth, hippocampal LTP and neurotransmitter release, and the postsynaptic protein neurogranin (a.k.a. RC3, BICKS and p17) which function remains to be determined. This review will focus on the protein kinase C activity in pre- and postsynaptic compartment during the early phase of LTP and the possible involvement of its substrates B-50 and neurogranin.
长时程增强（LTP）是一种用于研究突触可塑性的活动依赖性增强的著名实验模型，由于其持续时间长且具有关联性，它被提议作为一种研究记忆形成分子机制的系统。目前，有几条证据表明突触前和突触后激酶及其特定底物参与了LTP的分子机制。许多研究聚焦于蛋白激酶C（PKC）的参与情况。研究PKC在长时程增强中作用的一种方法是在海马切片原位磷酸化后确定其底物的磷酸化程度。两个可能的靶点是突触前膜相关蛋白B-50（又名GAP 43、神经调节蛋白和F1），它与大脑中不同形式的突触可塑性有关，如神经突生长、海马LTP和神经递质释放，以及突触后蛋白神经颗粒素（又名RC3、BICKS和p17），其功能尚待确定。本综述将聚焦于长时程增强早期突触前和突触后区室中的蛋白激酶C活性及其底物B-50和神经颗粒素的可能参与情况。
