Mechanisms controlling the trafficking, localization, and abundance of presynaptic Ca2+ channels
Name
fnmol-15-1116729.pdf
Size
3.69 MB
Format
Adobe PDF
Checksum (MD5)
44967ded67b4cd569af9a54b4962493e
Author(s)
Cunningham, Karen L.
Littleton, J. Troy
Date Issued
January 13, 2023
Publisher
Frontiers Media SA
Citation
Cunningham, Karen L. and Littleton, J. Troy. 2023. "Mechanisms controlling the trafficking, localization, and abundance of presynaptic Ca2+ channels." 15.
Version
Final published version
Abstract
Voltage-gated Ca2+ channels (VGCCs) mediate Ca2+ influx to trigger neurotransmitter release at specialized presynaptic sites termed active zones (AZs). The abundance of VGCCs at AZs regulates neurotransmitter release probability (Pr), a key presynaptic determinant of synaptic strength. Given this functional significance, defining the processes that cooperate to establish AZ VGCC abundance is critical for understanding how these mechanisms set synaptic strength and how they might be regulated to control presynaptic plasticity. VGCC abundance at AZs involves multiple steps, including channel biosynthesis (transcription, translation, and trafficking through the endomembrane system), forward axonal trafficking and delivery to synaptic terminals, incorporation and retention at presynaptic sites, and protein recycling. Here we discuss mechanisms that control VGCC abundance at synapses, highlighting findings from invertebrate and vertebrate models.
Subjects
Cellular and Molecular Neuroscience
Molecular Biology
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Terms of Use
Creative Commons Attribution 4.0 International license
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.3389/fnmol.2022.1116729
