Laboratory of Functional Neuroscience, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, Nara 630-0192, Japan.
J Chem Neuroanat. 2011 Sep;42(1):24-9. doi: 10.1016/j.jchemneu.2011.05.014. Epub 2011 Jun 6.
Accumulating evidence has suggested pivotal roles for neural proteases in development, maturation, aging, and cognitive functions. Among such proteases, neuropsin, a kallikrein gene-related (KLK) endoprotease, appears to have a significant plasticity function that has been analyzed primarily in the hippocampal Schaffer-collateral pathway. In this article, after reviewing the general features of neuropsin, its role in Schaffer-collateral synaptic plasticity is discussed in some detail. Enzymatically active neuropsin is necessary to establish the early phase of long-term potentiation (LTP). This type of LTP, which can be elicited by rather weak tetanic stimulation, is significant in synaptic late association between two independent hippocampal synapses. Neuropsin deficiency completely impaired the early phase of LTP, leading to the absence of late associativity. Associations between early and persistent-LTP synapses may be related to mammalian working memory and consequently integration in learning and memory.
越来越多的证据表明神经蛋白酶在发育、成熟、衰老和认知功能中起着关键作用。在这些蛋白酶中，神经蛋白酶是一种激肽释放酶相关的（KLK）内切蛋白酶，似乎具有重要的可塑性功能，主要在海马沙费尔- collateral 通路中进行分析。在本文中，在回顾神经蛋白酶的一般特征后，详细讨论了其在沙费尔 collateral 突触可塑性中的作用。具有酶活性的神经蛋白酶对于建立长时程增强（LTP）的早期阶段是必要的。这种可以通过相当弱的强直刺激引发的 LTP 类型在两个独立的海马突触之间的突触晚期关联中非常重要。神经蛋白酶缺乏完全损害了 LTP 的早期阶段，导致晚期关联性缺失。早期和持续 LTP 突触之间的关联可能与哺乳动物的工作记忆有关，因此与学习和记忆的整合有关。
