title: Endocytosis and synaptic plasticity: might the tail wag the dog?
abstract: In nerve terminals, endocytosis in compensation for transmitter exocytosis was once thought 'housekeeping'. Now, several lines of research utilizing optical endocytic probes have coalesced into a new functional model. The model comprises two distinct endocytosis and vesicle-processing paradigms that are differentially regulated in response to demand for transmitter. Under some circumstances, such as recovery from short-term depression, it appears that endocytosis, and not exocytosis, is rate-limiting for transmitter release and is therefore a principal determinant of synaptic strength.
authors.affiliation: Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA. wilk@cellbio.wustl.edu
authors.forename: Robert S
authors.initials: RS
authors.lastname: Wilkinson
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Lin
mesh_terms: D000818:Animals; D004705:Endocytosis / Q000502:physiology*; D005456:Fluorescent Dyes / Q000493:pharmacokinetics; D006801:Humans; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011726:Pyridinium Compounds / Q000493:pharmacokinetics; D000644:Quaternary Ammonium Compounds / Q000493:pharmacokinetics; D015398:Signal Transduction / Q000502:physiology; D013569:Synapses / Q000378:metabolism*; D013572:Synaptic Vesicles / Q000378:metabolism
chemical_list: C073804:FM1 43; D005456:Fluorescent Dyes; D018377:Neurotransmitter Agents; D011726:Pyridinium Compounds; D000644:Quaternary Ammonium Compounds