2005 Fiscal Year Final Research Report Summary
Synaptic vesicle recycling and changes in synaptic efficacy
| Project/Area Number |
16300130
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Gunma University |
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Principal Investigator |
KUROMI Hiroshi Gunma University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (30009633)
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| Co-Investigator(Kenkyū-buntansha) |
UENO Kohei Gunma University, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (40332556)
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| Project Period (FY) |
2004 – 2005
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| Keywords | synaptic vesicle / recycling / endocytosis / drosophila / exocytosis / channel / active-zone / La3+ |
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| Research Abstract |
We wish to clarify mechanisms of endocytosis of synaptic vesicles and roles of endocytosis in synaptic transmission at Drosophila Neuromuscular junction.
1. It has been believed that exocytosis and endocytosis of synaptic vesicles are controlled by the same Ca2+ influx, because endocytosis always follows exocytosis and both process require external Ca2+. We found that La3+ and fulunarizine, Ca2+ channel blocker, depressed endocytosis without affecting exocytosis, while PLTXII, Ca2+ channel blocker from spider toxin, depressed predominantly exocytosis. These results suggest that Ca2+ influx through distinct routes controls exocytosis and endocytosis.
2. Using Ca2+ channel blockers, we revealed two distinct endocytosis; active-zone endocytosis and non-active-zone endocytosis. Active-zone endocytosis is clathrin-independent and operate early phase of high activity, whereas non-active-zone endocytosis is clathrin-dependent and works in late phase of high activity. These results suggest that synaptic transmission at high activity is maintained coordinately by two types of endocytosis.
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