期刊
NEUROSCIENTIST
卷 8, 期 6, 页码 524-531出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1073858402238511
关键词
BDNF; docked vesicles; fusion pore; hippocampus; mEPSC; Poisson stimulation; quantal release; SNARE proteins; synaptic vesicles; TrkB; voltage-gated Ca2+ channels
资金
- NEI NIH HHS [EY-12782, R01 EY012782] Funding Source: Medline
- NICHD NIH HHS [P30-HD38985, P30 HD038985, P01-HD38760, P01 HD038760] Funding Source: Medline
- NINDS NIH HHS [R01 NS040593, R01 NS040593-09, R01-NS40593] Funding Source: Medline
- NINR NIH HHS [NRSA-09770] Funding Source: Medline
The neurotrophins (NTs) have recently been shown to elicit pronounced effects on quantal neurotransmitter release at both central and peripheral nervous system synapses. Due to their activity-dependent release, as well as the subcellular localization of both protein and receptor, NTs are ideally suited to modify the strength of neuronal connections by fine-tuning synaptic activity through direct actions at presynaptic terminals. Here, using BDNF as a prototypical example, the authors provide an update of recent evidence demonstrating that NTs enhance quantal neurotransmitter release at synapses through presynaptic mechanisms. The authors further propose that a potential target for NT actions at presynaptic terminals is the mechanism by which terminals retrieve synaptic vesicles after exocytosis. Depending on the temporal demands placed on synapses during high-frequency synaptic transmission, synapses may use two alternative modes of synaptic vesicle retrieval, the conventional slow endosomal recycling or a faster rapid retrieval at the active zone, referred to as kiss-and-run. By modulating Ca2+ microdomains associated with voltage-gated Ca2+ channels at active zones, NTs may elicit a switch from the slow to the fast mode of endocytosis of vesicles at presynaptic terminals during high-frequency synaptic transmission, allowing more reliable information transfer and neuronal signaling in the central nervous system.
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