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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Intermediate-term memory for site-specific sensitization in aplysia is maintained by persistent activation of protein kinase C.
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Intermediate-term memory for site-specific sensitization in aplysia is maintained by persistent activation of protein kinase C.

机译：通过蛋白激酶C的持续活化来维持海兔中特定部位致敏的中期记忆。

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Recent studies of long-term synaptic plasticity and long-term memory have demonstrated that the same functional endpoint, such as long-term potentiation, can be induced through distinct signaling pathways engaged by different patterns of stimulation. A critical question raised by these studies is whether different induction pathways either converge onto a common molecular mechanism or engage different molecular cascades for the maintenance of long-term plasticity. We directly examined this issue in the context of memory for sensitization in the marine mollusk Aplysia. In this system, training with a single tail shock normally induces short-term memory (<30 min) for sensitization of tail-elicited siphon withdrawal, whereas repeated spaced shocks induce both intermediate-term memory (ITM) (>90 min) and long-term memory (>24 hr). We now show that a single tail shock can also induce ITM that is expressed selectively at the trained site (site-specific ITM). Although phenotypically similar to the form of ITMinduced by repeated trials, the mechanisms by which site-specific ITM is induced and maintained are distinct. Unlike repeated-trial ITM, site-specific ITM requires neither protein synthesis nor PKA activity for induction or maintenance. Rather, the induction of site-specific ITM requires calpain-dependent proteolysis of activated PKC, yielding a persistently active PKC catalytic fragment (PKM) that also serves to maintain the memory in the intermediateterm temporal domain. Thus, two unique forms of ITM that have different induction requirements also use distinct molecular mechanisms for their maintenance.
机译：长期的突触可塑性和长期记忆的最新研究表明，可以通过不同刺激模式参与的不同信号通路来诱导相同的功能终点（例如长期增强）。这些研究提出的一个关键问题是，不同的诱导途径是否会融合到一个共同的分子机制上，或者参与维持长期可塑性的不同分子级联。我们直接在海洋软体动物海豚的记忆中研究了这个问题。在该系统中，单次尾部冲击训练通常会引起短期记忆（<30分钟），以敏化尾部引出的虹吸，而反复间隔的冲击会诱发中期记忆（ITM）（> 90分钟）和长时记忆长期记忆（> 24小时）。现在，我们显示单个尾巴电击也可以诱导在受过训练的部位（特定部位的ITM）选择性表达的ITM。尽管在表型上类似于重复试验诱导的ITM形式，但诱导和维持位点特异性ITM的机制却截然不同。与重复试验ITM不同，位点特异性ITM不需要蛋白质合成或PKA活性即可诱导或维持。相反，位点特异性ITM的诱导需要钙蛋白酶依赖的活化PKC的蛋白水解作用，产生持久活性的PKC催化片段（PKM），该片段还用于在中期时域内保持记忆。因此，具有不同诱导要求的ITM的两种独特形式也使用不同的分子机制进行维护。

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