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Regulation of synaptic release‐site Ca 2+ channel coupling as a mechanism to control release probability and short‐term plasticity
Author(s) -
Böhme Mathias A.,
Grasskamp Andreas T.,
Walter Alexander M.
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13188
Subject(s) - neurotransmission , synapse , synaptic vesicle , coupling (piping) , active zone , synaptic plasticity , neurotransmitter , biophysics , neuroscience , biology , chemistry , microbiology and biotechnology , vesicle , membrane , biochemistry , materials science , receptor , central nervous system , metallurgy
Synaptic transmission relies on the rapid fusion of neurotransmitter‐containing synaptic vesicles ( SV s), which happens in response to action potential ( AP )‐induced Ca 2+ influx at active zones ( AZ s). A highly conserved molecular machinery cooperates at SV ‐release sites to mediate SV plasma membrane attachment and maturation, Ca 2+ sensing, and membrane fusion. Despite this high degree of conservation, synapses – even within the same organism, organ or neuron – are highly diverse regarding the probability of AP s to trigger SV fusion. Additionally, repetitive activation can lead to either strengthening or weakening of transmission. In this review, we discuss mechanisms controlling release probability and this short‐term plasticity. We argue that an important layer of control is exerted by evolutionarily conserved AZ scaffolding proteins, which determine the coupling distance between SV fusion sites and voltage‐gated Ca 2+ channels ( VGCC ) and, thereby, shape synapse‐specific input/output behaviors. We propose that AZ ‐scaffold modifications may occur to adapt the coupling distance during synapse maturation and plastic regulation of synapse strength.