Endocytosis and synaptic plasticity: might the tail wag the dog?
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.
Wilkinson
Robert S
RS
Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA. wilk@cellbio.wustl.edu
Lin
Michael Y
MY
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
C073804:FM1 43; D005456:Fluorescent Dyes; D018377:Neurotransmitter Agents; D011726:Pyridinium Compounds; D000644:Quaternary Ammonium Compounds