Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons

Abstract Kinases play critical roles in synaptic and neuronal changes involved in the formation of memory. However, significant gaps exist in the understanding of how interactions among kinase pathways contribute to the mechanistically distinct temporal domains of memory ranging from short-term memo...

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Autores principales:	Yili Zhang, Paul D. Smolen, Leonard J. Cleary, John H. Byrne
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2f0a01c4d61d455fa22bb029442d5f0b
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spelling	oai:doaj.org-article:2f0a01c4d61d455fa22bb029442d5f0b2021-12-02T16:26:23ZQuantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons10.1038/s41598-021-94393-02045-2322https://doaj.org/article/2f0a01c4d61d455fa22bb029442d5f0b2021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94393-0https://doaj.org/toc/2045-2322Abstract Kinases play critical roles in synaptic and neuronal changes involved in the formation of memory. However, significant gaps exist in the understanding of how interactions among kinase pathways contribute to the mechanistically distinct temporal domains of memory ranging from short-term memory to long-term memory (LTM). Activation of protein kinase A (PKA) and mitogen-activated protein kinase (MAPK)—ribosomal S6 kinase (RSK) pathways are critical for long-term enhancement of neuronal excitability (LTEE) and long-term synaptic facilitation (LTF), essential processes in memory formation. This study provides new insights into how these pathways contribute to the temporal domains of memory, using empirical and computational approaches. Empirical studies of Aplysia sensory neurons identified a positive feedforward loop in which the PKA and ERK pathways converge to regulate RSK, and a negative feedback loop in which p38 MAPK inhibits the activation of ERK and RSK. A computational model incorporated these findings to simulate the dynamics of kinase activity produced by different stimulus protocols and predict the critical roles of kinase interactions in the dynamics of these pathways. These findings may provide insights into the mechanisms underlying aberrant synaptic plasticity observed in genetic disorders such as RASopathies and Coffin-Lowry syndrome.Yili ZhangPaul D. SmolenLeonard J. ClearyJohn H. ByrneNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-21 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yili Zhang Paul D. Smolen Leonard J. Cleary John H. Byrne Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons
description	Abstract Kinases play critical roles in synaptic and neuronal changes involved in the formation of memory. However, significant gaps exist in the understanding of how interactions among kinase pathways contribute to the mechanistically distinct temporal domains of memory ranging from short-term memory to long-term memory (LTM). Activation of protein kinase A (PKA) and mitogen-activated protein kinase (MAPK)—ribosomal S6 kinase (RSK) pathways are critical for long-term enhancement of neuronal excitability (LTEE) and long-term synaptic facilitation (LTF), essential processes in memory formation. This study provides new insights into how these pathways contribute to the temporal domains of memory, using empirical and computational approaches. Empirical studies of Aplysia sensory neurons identified a positive feedforward loop in which the PKA and ERK pathways converge to regulate RSK, and a negative feedback loop in which p38 MAPK inhibits the activation of ERK and RSK. A computational model incorporated these findings to simulate the dynamics of kinase activity produced by different stimulus protocols and predict the critical roles of kinase interactions in the dynamics of these pathways. These findings may provide insights into the mechanisms underlying aberrant synaptic plasticity observed in genetic disorders such as RASopathies and Coffin-Lowry syndrome.
format	article
author	Yili Zhang Paul D. Smolen Leonard J. Cleary John H. Byrne
author_facet	Yili Zhang Paul D. Smolen Leonard J. Cleary John H. Byrne
author_sort	Yili Zhang
title	Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons
title_short	Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons
title_full	Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons
title_fullStr	Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons
title_full_unstemmed	Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons
title_sort	quantitative description of the interactions among kinase cascades underlying long-term plasticity of aplysia sensory neurons
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/2f0a01c4d61d455fa22bb029442d5f0b
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Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons

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