Inhibition of protein kinase C affects on mode of synaptic vesicle exocytosis due to cholesterol depletion.
Biochem Biophys Res Commun
; 456(1): 145-50, 2015 Jan 02.
Article
em En
| MEDLINE
| ID: mdl-25446113
ABSTRACT
Previous studies demonstrated that depletion of membrane cholesterol by 10mM methyl-beta-cyclodextrin (MCD) results in increased spontaneous exocytosis at both peripheral and central synapses. Here, we investigated the role of protein kinase C in the enhancement of spontaneous exocytosis at frog motor nerve terminals after cholesterol depletion using electrophysiological and optical methods. Inhibition of the protein kinase C by myristoylated peptide and chelerythrine chloride prevented MCD-induced increases in FM1-43 unloading, whereas the frequency of spontaneous postsynaptic events remained enhanced. The increase in FM1-43 unloading still could be observed if sulforhodamine 101 (the water soluble FM1-43 quencher that can pass through the fusion pore) was added to the extracellular solution. This suggests a possibility that exocytosis of synaptic vesicles under these conditions could occur through the kiss-and-run mechanism with the formation of a transient fusion pore. Inhibition of phospholipase C did not lead to similar change in MCD-induced exocytosis.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Vesículas Sinápticas
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Proteína Quinase C
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Colesterol
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Inibidores Enzimáticos
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Exocitose
Limite:
Animals
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article