@article{0690ee0ffd22411b8f39ca70bc007436,
title = "The Drosophila postsynaptic DEG/ENaC channel ppk29 contributes to excitatory neurotransmission",
abstract = "The protein family of degenerin/epithelial sodium channels (DEG/ENaCs) is composed of diverse animal-specific, non-voltage-gated ion channels that play important roles in regulating cationic gradients across epithelial barriers. Some family members are also enriched in neural tissues in both vertebrates and invertebrates. However, the specific neurophysiological functions of most DEG/ENaC-encoding genes remain poorly understood. The fruit fly Drosophila melanogaster is an excellent model for deciphering the functions of DEG/ENaC genes because its genome encodes an exceptionally large number of DEG/ENaC subunits termed pickpocket (ppk) 1-31. Here we demonstrate that ppk29 contributes specifically to the postsynaptic modulation of excitatory synaptic transmission at the larval neuromuscular junction. Electrophysiological data indicate that the function of ppk29 in muscle is necessary for normal postsynaptic responsivity to neurotransmitter release and for normal coordinated larval movement. The ppk29 mutation does not affect gross synaptic morphology and ultrastructure, which indicates that the observed phenotypes are likely due to defects in glutamate receptor function. Together, our data indicate that DEG/ENaC ion channels play a fundamental role in the postsynaptic regulation of excitatory neurotransmission.",
keywords = "DEG/ENaC, Drosophila melanogaster, Fruit fly, NMJ, Synapse",
author = "Alexis Hill and Xingguo Zheng and Xiling Li and Ross McKinney and Dion Dickman and Yehuda Ben-Shahar",
note = "Funding Information: This work was supported by W.M. Keck and McDonnell Center Postdoctoral Fellowships to A.H.; National Institutes of Health (NIH) Grant NS-019546 and research fellowships from the Alfred P. Sloan, Ellison Medical, the Whitehall, Klingenstein-Simons, and Mallinckrodt Foundations to D.D.; and grants from the Klingenstein Foundation and the McDonnell Center for Cellular and Molecular Neurobiology, and NIH Grant 5R21-NS-089834 to Y.B.-S. We thank Aaron DiAntonio for antibodies; and the Bloomington Drosophila Stock Center at Indiana University and the fly community for fly strains. Anti-BRP and anti-GluRIIA antibodies, developed by E. Buchner and C. Goodman, respectively, were from the Developmental Studies Hybridoma Bank at the University of Iowa, Department of Biology. We also thank Matthew Joens and James Fitzpatrick from the Washington University in St. Louis Center for Cellular Imaging, which is supported by the Washington University in St. Louis School of Medicine, The Children{\textquoteright}s Discovery Institute of Washington University in St. Louis and St. Louis Children{\textquoteright}s Hospital, the Foundation for Barnes-Jewish Hospital, the National Institute for Neurological Disorders and Stroke (Grant NS-086741), the Office of the NIH Director (Grant OD-021694), and the National Science Foundation (Grant 1633971). Publisher Copyright: {\textcopyright} 2017 the authors.",
year = "2017",
month = mar,
day = "22",
doi = "10.1523/JNEUROSCI.3850-16.2017",
language = "English",
volume = "37",
pages = "3171--3180",
journal = "Journal of Neuroscience",
issn = "0270-6474",
number = "12",
}