Title : Regulation of presynaptic strength by controlling Ca2+ channel mobility: effects of cholesterol depletion on release at the cone ribbon synapse.

Pub. Date : 2012 Jun

PMID : 22442573






5 Functional Relationships(s)
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1 Using single-particle tracking techniques, we measured the expansion of Ca(V) channel confinement domains caused by depletion of membrane cholesterol with cholesterol oxidase or methyl-beta-cyclodextrin. Cholesterol carbonic anhydrase 5A Homo sapiens
2 Using single-particle tracking techniques, we measured the expansion of Ca(V) channel confinement domains caused by depletion of membrane cholesterol with cholesterol oxidase or methyl-beta-cyclodextrin. methyl-beta-cyclodextrin carbonic anhydrase 5A Homo sapiens
3 Replenishing cholesterol restored Ca(V) channel domain size and release efficiency to control levels. Cholesterol carbonic anhydrase 5A Homo sapiens
4 Furthermore, the finding that cholesterol depletion impairs coupling between channel opening and vesicle release by allowing Ca(V) channels to move further from release sites shows that changes in presynaptic Ca(V) channel mobility can be a mechanism for adjusting synaptic strength. Cholesterol carbonic anhydrase 5A Homo sapiens
5 Furthermore, the finding that cholesterol depletion impairs coupling between channel opening and vesicle release by allowing Ca(V) channels to move further from release sites shows that changes in presynaptic Ca(V) channel mobility can be a mechanism for adjusting synaptic strength. Cholesterol carbonic anhydrase 5A Homo sapiens