The molecular physiology of activity-dependent bulk endocytosis of synaptic vesicles
Article first published online: 16 SEP 2009
© 2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry
Journal of Neurochemistry
Volume 111, Issue 4, pages 901–914, November 2009
How to Cite
Clayton, E. L. and Cousin, M. A. (2009), The molecular physiology of activity-dependent bulk endocytosis of synaptic vesicles. Journal of Neurochemistry, 111: 901–914. doi: 10.1111/j.1471-4159.2009.06384.x
- Issue published online: 16 OCT 2009
- Article first published online: 16 SEP 2009
- Received June 19, 2009; revised manuscript received August 6, 2009; accepted August 31, 2009.
- synaptic vesicle
Central nerve terminals release neurotransmitter in response to a wide variety of stimuli. Because maintenance of neurotransmitter release is dependent on the continual supply of synaptic vesicles (SVs), nerve terminals possess an array of endocytosis modes to retrieve and recycle SV membrane and proteins. During mild stimulation conditions, single SV retrieval modes such as clathrin-mediated endocytosis predominate. However, during increased neuronal activity, additional SV retrieval capacity is required, which is provided by activity-dependent bulk endocytosis (ADBE). ADBE is the dominant SV retrieval mechanism during elevated neuronal activity. It is a high capacity SV retrieval mode that is immediately triggered during such stimulation conditions. This review will summarize the current knowledge regarding the molecular mechanism of ADBE, including molecules required for its triggering and subsequent steps, including SV budding from bulk endosomes. The molecular relationship between ADBE and the SV reserve pool will also be discussed. It is becoming clear that an understanding of the molecular physiology of ADBE will be of critical importance in attempts to modulate both normal and abnormal synaptic function during intense neuronal activity.