Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function

Since the discovery of nerve growth factor (NGF) more than a half century ago (Levi-Montalcini and Cohen, 1960), the prototypic neurotrophin family has included brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Neurotrophins bind to the Trk family of recepto...

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Main Authors: Yoshii, Akira, Constantine-Paton, Martha, Ip, Nancy Y.
Other Authors: Massachusetts Institute of Technology. Department of Biology
Format: Article
Language:en_US
Published: Frontiers Research Foundation 2015
Online Access:http://hdl.handle.net/1721.1/98181
https://orcid.org/0000-0003-2268-0863
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author Yoshii, Akira
Constantine-Paton, Martha
Ip, Nancy Y.
author2 Massachusetts Institute of Technology. Department of Biology
author_facet Massachusetts Institute of Technology. Department of Biology
Yoshii, Akira
Constantine-Paton, Martha
Ip, Nancy Y.
author_sort Yoshii, Akira
collection MIT
description Since the discovery of nerve growth factor (NGF) more than a half century ago (Levi-Montalcini and Cohen, 1960), the prototypic neurotrophin family has included brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Neurotrophins bind to the Trk family of receptors, as well as the p75 receptor, to activate multiple intracellular signaling cascades (reviewed by Reichardt, 2006). BDNF receptor tropomyosin receptor kinase B (TrkB) signaling has been extensively studied for its roles in the central nervous system (CNS) ranging from cell survival, axonal and dendritic growth and synapse formation. The pathway mediates long-lasting activity-modulated synaptic changes on excitatory and inhibitory neurons and plays critical roles in circuit development and maintenance. In addition to BDNF, many studies have identified other “growth” or signaling factors in the CNS that play important roles in the development, maintenance, and control of synaptic and circuit function. However, details of the intracellular signaling systems downstream of these events are frequently unexplored. In this Research Topic, we have collected original studies and review articles that present cellular and molecular mechanisms concerning activity-dependent synapse formation and their implications for behavior and brain disorders.
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spelling mit-1721.1/981812022-10-01T17:12:02Z Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function Yoshii, Akira Constantine-Paton, Martha Ip, Nancy Y. Massachusetts Institute of Technology. Department of Biology Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences McGovern Institute for Brain Research at MIT Constantine-Paton, Martha Since the discovery of nerve growth factor (NGF) more than a half century ago (Levi-Montalcini and Cohen, 1960), the prototypic neurotrophin family has included brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Neurotrophins bind to the Trk family of receptors, as well as the p75 receptor, to activate multiple intracellular signaling cascades (reviewed by Reichardt, 2006). BDNF receptor tropomyosin receptor kinase B (TrkB) signaling has been extensively studied for its roles in the central nervous system (CNS) ranging from cell survival, axonal and dendritic growth and synapse formation. The pathway mediates long-lasting activity-modulated synaptic changes on excitatory and inhibitory neurons and plays critical roles in circuit development and maintenance. In addition to BDNF, many studies have identified other “growth” or signaling factors in the CNS that play important roles in the development, maintenance, and control of synaptic and circuit function. However, details of the intracellular signaling systems downstream of these events are frequently unexplored. In this Research Topic, we have collected original studies and review articles that present cellular and molecular mechanisms concerning activity-dependent synapse formation and their implications for behavior and brain disorders. National Institutes of Health (U.S.) (Grant 5R01EY006039-27) National Institutes of Health (U.S.) (Grant 5R01EY014074-15) 2015-08-21T14:42:34Z 2015-08-21T14:42:34Z 2015-06 2015-05 Article http://purl.org/eprint/type/JournalArticle 1663-3563 http://hdl.handle.net/1721.1/98181 Yoshii, Akira, Martha Constantine-Paton, and Nancy Y. Ip. “Editorial: Cell and Molecular Signaling, and Transport Pathways Involved in Growth Factor Control of Synaptic Development and Function.” Frontiers in Synaptic Neuroscience 7 (June 4, 2015). https://orcid.org/0000-0003-2268-0863 en_US http://dx.doi.org/10.3389/fnsyn.2015.00008 Frontiers in Synaptic Neuroscience Creative Commons Attribution http://creativecommons.org/licenses/by/4.0/ application/pdf Frontiers Research Foundation Frontiers Research Foundation
spellingShingle Yoshii, Akira
Constantine-Paton, Martha
Ip, Nancy Y.
Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function
title Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function
title_full Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function
title_fullStr Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function
title_full_unstemmed Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function
title_short Editorial: Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function
title_sort editorial cell and molecular signaling and transport pathways involved in growth factor control of synaptic development and function
url http://hdl.handle.net/1721.1/98181
https://orcid.org/0000-0003-2268-0863
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