ArticleDevelopmental neurobiology2014
Distinct roles of Drosophila cacophony and Dmca1D Ca(2+) channels in synaptic homeostasis: genetic interactions with slowpoke Ca(2+) -activated BK channels in presynaptic excitability and postsynaptic response.
Article in Developmental neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 35 citations in OpenAlex.
- Pro-tumoral CaScientific reports · 2026Article
- Regulation of excitation-contraction coupling at the Drosophila neuromuscular junction.The Journal of physiology · 2022Article
- Stac protein regulates release of neuropeptides.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Depressed neuromuscular transmission causes weakness in mice lacking BK potassium channels.The Journal of general physiology · 2020Article
- Deletion of a specific exon in the voltage-gated calcium channel geneThe Journal of experimental biology · 2019Article
- Inter-relationships among physical dimensions, distal-proximal rank orders, and basal GCaMP fluorescence levels in CaJournal of neurogenetics · 2018Article
- Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.PLoS genetics · 2018Article
- Drosophila Voltage-Gated Calcium Channel α1-Subunits Regulate Cardiac Function in the Aging Heart.Scientific reports · 2018Article
- Differential contribution of CaThe Journal of general physiology · 2018Article
- Restoration of Motor Defects Caused by Loss ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Nonreciprocal homeostatic compensation inJournal of neurophysiology · 2017Article
- Transient voltage-activated KJournal of neurophysiology · 2017Article
- Survival and growth of C57BL/6J mice lacking the BK channel,Physiological reports · 2017Article
- Identification of Splicing Quantitative Trait Loci (sQTL) inFrontiers in genetics · 2017Article
- Cyclic nucleotide signaling is required during synaptic refinement at the Drosophila neuromuscular junction.Developmental neurobiology · 2017Article
- Presynaptic BK channels control transmitter release: physiological relevance and potential therapeutic implications.The Journal of physiology · 2016Review
- Properties and physiological function of Ca2+-dependent K+ currents in uniglomerular olfactory projection neurons.Journal of neurophysiology · 2016Article
- Transient BK outward current enhances motoneurone firing rates during Drosophila larval locomotion.The Journal of physiology · 2015Article
- Store-Operated Calcium Entry through Orai Is Required for Transcriptional Maturation of the Flight Circuit in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- The role of cAMP in synaptic homeostasis in response to environmental temperature challenges and hyperexcitability mutations.Frontiers in cellular neuroscience · 2015Article
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3 authors at 2 institutions in 2 countries.
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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 (CaV 2) and Dmca1D (CaV 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. postsynaptic 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.
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