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Distinct roles of Drosophila cacophony and Dmca1D Ca2+ channels in synaptic homeostasis: Genetic interactions with slowpoke Ca2+-activated BK channels in presynaptic excitability and postsynaptic response
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Distinct roles of Drosophila cacophony and Dmca1D Ca2+ channels in synaptic homeostasis: Genetic interactions with slowpoke Ca2+-activated BK channels in presynaptic excitability and postsynaptic response

Jihye Lee, Atsushi Ueda and Chun-Fang Wu
Developmental neurobiology (Hoboken, N.J.), Vol.74(1), pp.1-15
01/2014
DOI: 10.1002/dneu.22120
PMCID: PMC3859705
PMID: 23959639
url
http://doi.org/10.1002/dneu.22120View
Open Access

Abstract

Ca 2+ influx through voltage-activated Ca 2+ channels and its feedback regulation by Ca 2+ -activated K + (BK) channels is critical in Ca 2+ -dependent cellular processes, including synaptic transmission, growth and homeostasis. Here we report differential roles of cacophony (Ca V 2) and Dmca1D (Ca V 1) Ca 2+ channels in synaptic transmission and in synaptic homeostatic regulations induced by slowpoke ( slo ) BK channel mutations. At Drosophila larval neuromuscular junctions (NMJs), a well-established homeostatic mechanism of transmitter release enhancement is triggered by experimentally suppressing postsynaptic receptor response. In contrast, a distinct homeostatic adjustment is induced by slo mutations. To compensate for the loss of BK channel control presynaptic Sh K + current is upregulated to suppress transmitter release, coupled with a reduction in quantal size. We demonstrate contrasting effects of cac and Dmca1D channels in decreasing transmitter release and muscle excitability, respectively, consistent with their predominant pre- vs. post-synaptic localization. Antibody staining indicated reduced postsynaptic GluRII receptor subunit density and altered ratio of GluRII A and B subunits in slo NMJs, leading to quantal size reduction. Such slo -triggered modifications were suppressed in cac;;slo larvae, correlated with a quantal size reversion to normal in double mutants, indicating a role of cac Ca 2+ channels in slo -triggered homeostatic processes. In Dmca1D;slo double mutants, the quantal size and quantal content were not drastically different from those of slo , although Dmca1D suppressed the slo -induced satellite bouton overgrowth. Taken together, cac and Dmca1D Ca 2+ channels differentially contribute to functional and structural aspects of slo -induced synaptic modifications.
spontaneous vesicle release Synaptic transmission mEJPs slowpoke (BK) larval neuromuscular junction (NMJ) Dmca1D (CaV1) EJPs cacophony (CaV2) synaptic homeostasis

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