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Lee, J., Wu, C.F. (2010). Orchestration of stepwise synaptic growth by k+ and Ca2+ channels in Drosophila.  J. Neurosci. 30(47): 15821--15833.
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Research paper

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 Ca(2+)-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 Erg K(+) channels interact with separate sets of synaptic proteins to affect distinct growth steps. Post-synaptic L-type Ca(2+) channels, Dmca1D, and PSD-95-like scaffold protein, Discs large, are required for satellite budding induced by slowpoke and seizure mutations. Pre-synaptic cacophony Ca(2+) 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 Ca(2+)/CaM-dependent adenylyl cyclase, demonstrating a convergence of K(+) channels of different functional categories in regulation of excitability-dependent Ca(2+) influx for triggering cAMP-mediated growth plasticity.

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PMC3075884 (PMC) (EuropePMC)
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    Publication Type
    J. Neurosci.
    Journal of Neuroscience
    Publication Year
    0270-6474 1529-2401
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    Aberrations (1)
    Alleles (25)
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