Abstract:
: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 approximately 50%, and decrease synaptic area and the density of docked and clustered vesicles. Pre- but 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.
journal_name
Neuronjournal_title
Neuronauthors
Song W,Ranjan R,Dawson-Scully K,Bronk P,Marin L,Seroude L,Lin YJ,Nie Z,Atwood HL,Benzer S,Zinsmaier KEdoi
10.1016/s0896-6273(02)00932-7subject
Has Abstractpub_date
2002-09-26 00:00:00pages
105-19issue
1eissn
0896-6273issn
1097-4199pii
S0896627302009327journal_volume
36pub_type
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