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Role of p90 ribosomal S6 kinase in long-term synaptic facilitation and enhanced neuronal excitability.
Scientific Reports ( IF 3.8 ) Pub Date : 2020-01-17 , DOI: 10.1038/s41598-020-57484-y Rong-Yu Liu 1 , Yili Zhang 1 , Paul Smolen 1 , Leonard J Cleary 1 , John H Byrne 1
Scientific Reports ( IF 3.8 ) Pub Date : 2020-01-17 , DOI: 10.1038/s41598-020-57484-y Rong-Yu Liu 1 , Yili Zhang 1 , Paul Smolen 1 , Leonard J Cleary 1 , John H Byrne 1
Affiliation
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Multiple kinases converge on the transcription factor cAMP response element-binding protein (CREB) to enhance the expression of proteins essential for long-term synaptic plasticity and memory. The p90 ribosomal S6 kinase (RSK) is one of these kinases, although its role is poorly understood. The present study exploited the technical advantages of the Aplysia sensorimotor culture system to examine the role of RSK in long-term synaptic facilitation (LTF) and long-term enhancement of neuronal excitability (LTEE), two correlates of long-term memory (LTM). Inhibition of RSK expression or RSK activity both significantly reduced CREB1 phosphorylation, LTF, and LTEE, suggesting RSK is required for learning-related synaptic plasticity and enhancement in neuronal excitability. In addition, knock down of RSK by RNAi in Aplysia sensory neurons impairs LTF, suggesting that this may be a useful single-cell system to study aspects of defective synaptic plasticity in Coffin-Lowry Syndrome (CLS), a cognitive disorder that is caused by mutations in rsk2 and associated with deficits in learning and memory. We found that the impairments in LTF and LTEE can be rescued by a computationally designed spaced training protocol, which was previously demonstrated to augment normal LTF and LTM.
中文翻译：
p90核糖体S6激酶在长期突触促进和增强神经元兴奋性中的作用。
多种激酶在转录因子cAMP反应元件结合蛋白（CREB）上汇聚，以增强长期突触可塑性和记忆所必需的蛋白表达。尽管对p90核糖体S6激酶（RSK）的作用了解甚少，但它是其中的一种。本研究利用Aplysia感觉运动培养系统的技术优势来检查RSK在长期突触促进（LTF）和长期增强神经元兴奋性（LTEE）中的作用，这是长期记忆（LTM）的两个相关因素。抑制RSK表达或RSK活性均显着降低了CREB1的磷酸化，LTF和LTEE，这表明RSK是学习相关突触可塑性和增强神经元兴奋性所必需的。另外，海葵感官神经元中RNAi敲除RSK会损害LTF，提示这可能是一个有用的单细胞系统，用于研究棺材-低综合征（CLS）中突触可塑性缺陷的方面，这是一种由rsk2突变引起的认知障碍，与学习和记忆障碍有关。我们发现，可以通过计算设计的间隔训练协议来挽救LTF和LTEE中的损伤，该协议先前已证明可以增强正常LTF和LTM。
更新日期：2020-01-17
中文翻译：
p90核糖体S6激酶在长期突触促进和增强神经元兴奋性中的作用。
多种激酶在转录因子cAMP反应元件结合蛋白（CREB）上汇聚，以增强长期突触可塑性和记忆所必需的蛋白表达。尽管对p90核糖体S6激酶（RSK）的作用了解甚少，但它是其中的一种。本研究利用Aplysia感觉运动培养系统的技术优势来检查RSK在长期突触促进（LTF）和长期增强神经元兴奋性（LTEE）中的作用，这是长期记忆（LTM）的两个相关因素。抑制RSK表达或RSK活性均显着降低了CREB1的磷酸化，LTF和LTEE，这表明RSK是学习相关突触可塑性和增强神经元兴奋性所必需的。另外，海葵感官神经元中RNAi敲除RSK会损害LTF，提示这可能是一个有用的单细胞系统，用于研究棺材-低综合征（CLS）中突触可塑性缺陷的方面，这是一种由rsk2突变引起的认知障碍，与学习和记忆障碍有关。我们发现，可以通过计算设计的间隔训练协议来挽救LTF和LTEE中的损伤，该协议先前已证明可以增强正常LTF和LTM。
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