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Membrane cholesterol regulates different modes of synaptic vesicle release and retrieval at the frog neuromuscular junction
Author(s) -
Rodrigues Hermann A.,
Lima Ricardo F.,
Fonseca Matheus de C.,
Amaral Ernani A.,
Martinelli Patrícia M.,
Naves Lígia A.,
Gomez Marcus V.,
Kushmerick Christopher,
Prado Marco A. M.,
Guatimosim Cristina
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12300
Subject(s) - synaptic vesicle , vesicle , vesicle fusion , neuromuscular junction , synaptic vesicle recycling , biophysics , snap25 , biology , microbiology and biotechnology , chemistry , biochemistry , neuroscience , membrane
We investigated the effects of cholesterol removal on spontaneous and KC l‐evoked synaptic vesicle recycling at the frog neuromuscular junction. Cholesterol removal by methyl‐β‐cyclodextrin (Mβ CD ) induced an increase in the frequency of miniature end‐plate potentials ( MEPP s) and spontaneous destaining of synaptic vesicles labeled with the styryl dye FM 1‐43. Treatment with Mβ CD also increased the size of MEPP s without causing significant changes in nicotinic receptor clustering. At the ultrastructural level, synaptic vesicles from nerve terminals treated with Mβ CD were larger than those from control. In addition, treatment with Mβ CD reduced the fusion of synaptic vesicles that are mobilized during KC l‐evoked stimulation, but induced recycling of those vesicles that fuse spontaneously. We therefore suggest that Mβ CD might favor the release of vesicles that belong to a pool that is different from that involved in the KC l‐evoked release. These results reveal fundamental differences in the synaptic vesicle cycle for spontaneous and evoked release, and suggest that deregulation of cholesterol affects synaptic vesicle biogenesis and increases transmitter packing.