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K+ channel reorganization and homeostatic plasticity during postembryonic development: biophysical and genetic analyses in acutely dissociated Drosophila central neurons
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K+ channel reorganization and homeostatic plasticity during postembryonic development: biophysical and genetic analyses in acutely dissociated Drosophila central neurons

Taixiang Saur, I-Feng Peng, Peng Jiang, Neng Gong, Wei-Dong Yao, Tian-Le Xu and Chun-Fang Wu
Journal of neurogenetics, Vol.30(3-4), pp.259-275
10/01/2016
DOI: 10.1080/01677063.2016.1255212
PMCID: PMC5918286
PMID: 27868467
url
https://www.ncbi.nlm.nih.gov/pmc/articles/5918286View
Open Access

Abstract

Intrinsic electric activities of neurons play important roles in establishing and refining neural circuits during development. However, how the underlying ionic currents undergo postembryonic reorganizations remains largely unknown. Using acutely dissociated neurons from larval, pupal, and adult Drosophila brains, we show drastic re-assemblies and compensatory regulations of voltage-gated (I\nKv\n) and Ca\n2+\n-activated (I\nK(Ca)\n) K\n+ \ncurrents during postembryonic development. Larval and adult neurons displayed prominent fast-inactivating I\nKv\n, mediated by the Shaker (Sh) channel to a large extent, while in the same neurons I\nK(Ca)\nwas far smaller in amplitude. In contrast, pupal neurons were characterized by large sustained I\nKv\nand prominent I\nK(Ca)\n, encoded predominantly by the slowpoke (slo) gene. Surprisingly, deletion of Sh in the Sh\nM\nnull mutant removed inactivating, transient I\nKv\nfrom large portions of neurons at all stages. Interestingly, elimination of Sh currents was accompanied by upregulation of non-Sh transient I\nKv\n. In comparison, the slo\n1\nmutation abolished the vast majority of I\nK(Ca)\n, particularly at the pupal stage. Strikingly, the deficiency of I\nK(Ca)\nin slo pupae was compensated by the transient component of I\nKv\nmediated by Sh channels. Thus, I\nK(Ca)\nappears to play critical roles in pupal development and its absence induces functional compensations from a specific transient I\nKv\ncurrent. While mutants lacking either Sh or slo currents survived normally, Sh;;slo double mutants deficient in both failed to survive through pupal metamorphosis. Together, our data highlight significant reorganizations and homeostatic compensations of K\n+ \ncurrents during postembryonic development and uncover previously unrecognized roles for Sh and slo in this plastic process.
voltage-gated K current pupa Sh channels larva slo channels Whole-cell current adult activated K

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