Journal
FRONTIERS IN MOLECULAR NEUROSCIENCE
Volume 15, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2022.1116729
Keywords
voltage-gated calcium channel; synapse; active zone; neurotransmitter release; protein trafficking
Categories
Ask authors/readers for more resources
Voltage-gated Ca2+ channels (VGCCs) play a crucial role in regulating neurotransmitter release at synapses. The abundance of VGCCs at active zones directly impacts synaptic strength. This article discusses the mechanisms involved in establishing VGCC abundance at synapses, including channel biosynthesis, axonal trafficking, incorporation and retention at presynaptic sites, and protein recycling, with insights from both invertebrate and vertebrate models.
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 (P-r), 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available