Journal
NEURON
Volume 36, Issue 1, Pages 105-119Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(02)00932-7
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Funding
- NEI NIH HHS [EY09278] Funding Source: Medline
- NIA NIH HHS [AG16630] Funding Source: Medline
- NINDS NIH HHS [R01NS38274] Funding Source: Medline
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Regulation of synaptic strength is essential for neuronal information processing, but the molecular mechanisms that control changes in neuroexocytosis are only partially known. Here we show that the putative G protein-coupled receptor Methuselah (Mth) is required in the presynaptic motor neuron to acutely upregulate neurotransmitter exocytosis at larval Drosophila NMJs. Mutations in the mth gene reduce evoked neurotransmitter release by similar to50%, and decrease synaptic area and the density of docked and clustered vesicles. Prebut not postsynaptic expression of normal Mth restored normal release in mth mutants. Conditional expression of Mth restored normal release and normal vesicle docking and clustering but not the reduced size of synaptic sites, suggesting that Mth acutely adjusts vesicle trafficking to synaptic sites.
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