Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 47, Pages 15821-15833Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3448-10.2010
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Funding
- National Institutes of Health [NS 26528]
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Synapse formation is tightly associated with neuronal excitability. We found striking synaptic overgrowth caused by Drosophila K+-channel mutations of the seizure and slowpoke genes, encoding Erg and Ca2+-activated large-conductance (BK) channels, respectively. These mutants display two distinct patterns of satellite budding from larval motor terminus synaptic boutons. Double-mutant analysis indicates that BK and ErgK(+) channels interact with separate sets of synaptic proteins to affect distinct growth steps. Post-synaptic L-type Ca2+ channels, Dmca1D, and PSD-95-like scaffold protein, Discs large, are required for satellite budding induced by slowpoke and seizure mutations. Pre-synaptic cacophony Ca2+ channels and the NCAM-like adhesion molecule, Fasciclin II, take part in a maturation step that is partially arrested by seizure mutations. Importantly, slowpoke and seizure satellites were both suppressed by rutabaga mutations that disrupt Ca2+/CaM-dependent adenylyl cyclase, demonstrating a convergence of K+ channels of different functional categories in regulation of excitability-dependent Ca2+ influx for triggering cAMP-mediated growth plasticity.
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