The actin filament and dendritic peptide release.
F-actin remodelling has been implicated in regulated secretion from many cell types, in particular secretion from neuron axon terminals and neuroendocrine cell types. Cortical F-actin has long been postulated to act as a barrier to vesicle movement and hence to inhibit secretion; however, more recent studies point to F-actin remodelling providing both supporting and restraining roles in secretion. Magnocellular neurons of the supraoptic nucleus secrete either oxytocin or vasopressin from their dendrites as well as their axon terminals; and peptide release from these two compartments can be differentially controlled to allow secretion from one compartment in isolation from the other. While oxytocin and vasopressin secretion can be provoked by F-actin depolymerization in both compartments, acutely stimulated secretion is dependent on F-actin remodelling in dendrites but not axon terminals, suggesting that F-actin plays a different role in regulating the readily releasable pool of secretory vesicles in the two compartments. In addition, activity-dependent secretion from the dendritic compartment can be primed by prior exposure to agents, including oxytocin, that stimulate release of Ca(2+) from intracellular stores. While remodelling of F-actin is involved, it is not solely responsible for priming secretory responses.
Tobin
V A
VA
Centre for Integrative Physiology, University of Edinburgh, George Square, Edinburgh EH8 9XD, U.K.
Ludwig
M
M
D000199:Actins / Q000378:metabolism*; D003712:Dendrites / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism; D010455:Peptides / Q000378:metabolism*
D000199:Actins; D010455:Peptides