Local TrkB signaling: themes in development and neural plasticity
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REVIEW
Local TrkB signaling: themes in development and neural plasticity Aaron Johnstone 1 & William Mobley 1 Received: 19 June 2020 / Accepted: 10 August 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract The sensitivity of the nervous system to receive and respond to events, both internal and in the environment, depends on the ability of neural structures to remodel in response to experience (Kandel 2001; Mayford et al. 2012). Neural plasticity depends on rapid, tightly controlled rearrangements of cytoskeleton, membrane morphology, and protein content. Neurons regulate plasticity across orders of structural organization, from changes in molecular machinery that calls forth the synaptic alterations that underlie learning and memory, to events that evoke mesoscale alterations in neurite architecture, and to the birth and death of neurons. We address the concept that the events responsible for such diverse modification of neurons originate from local changes in signaling and that understanding the underlying mechanisms requires an appreciation of the nature of constraints placed upon spatial and temporal activity. During development and in the adult, both the remodeling of specific subcellular structures and induction of synaptic plasticity require local control and regulation of signaling, including those initiated by activation of surface receptors (Reichardt 2006). As an example, the receptor tyrosine kinase TrkB, activated by its ligand brain-derived neurotrophic factor (BDNF), has emerged as a potent modulator of plasticity in both development and adulthood, from neurite pruning and branching events during PNS and CNS development, to learning and memory. Here, we review the mechanisms by which TrkB signaling engages in local remodeling to support neural plasticity. Keywords TrkB . Brain derived neurotrophic factor . BDNF . Neurotrophin . Synaptic plasticity . Developmental degeneration . Local signaling . LTP . Long-term potentiation
Introduction Neural plasticity, or the ability of neurons and networks to change in response to outside events and endogenous developmental programs, enables the patterning of the developing nervous system and is registered as synaptic plasticity throughout adulthood to facilitate learning and memory (Kandel 2001). Intriguingly, events engaged during both development and in the adult require sensitive and rapid responsiveness to local molecular cues. Thus, for example, the earliest responses to receptor activation build on local intracellular responses. These events are regulated by a variety of factors and allow for both local events (Terenzio et al. 2017) and in some cases the support of cellular and tissue homeostasis. Throughout development and adulthood, paracrine and autocrine actions of a family of soluble ligands, the neurotrophins, * William Mobley [email protected] 1
Department of Neurosciences, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
and their cognate tyrosine kinase receptors, are major regulators of ne
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