Journal
NEURON
Volume 33, Issue 5, Pages 789-804Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(02)00601-3
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Funding
- NCI NIH HHS [CA46128] Funding Source: Medline
- NIDA NIH HHS [DA00436] Funding Source: Medline
- NIGMS NIH HHS [GM61925] Funding Source: Medline
- NIMH NIH HHS [MH25642] Funding Source: Medline
- NINDS NIH HHS [NS36251, NS24692] Funding Source: Medline
- Telethon [D.111] Funding Source: Medline
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The function of the clathrin coat in synaptic vesicle endocytosis is assisted by a variety of accessory factors, among which amphiphysin (amphiphysin 1 and 2) is one of the best characterized. A putative endocytic function of amphiphysin was supported by dominant-negative interference studies. We have now generated amphiphysin 1 knockout mice and found that lack of amphiphysin 1 causes a parallel dramatic reduction of amphiphysin 2 selectively in brain. Cell-free assembly of endocytic protein scaffolds is defective in mutant brain extracts. Knockout mice exhibit defects in synaptic vesicle recycling that are unmasked by stimulation and suggest impairments at multiple stages of the cycle. These defects correlate with increased mortality due to rare irreversible seizures and with major learning deficits, suggesting a critical role of amphiphysin for higher brain functions.
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