Knockdown of zebrafish Nav1.6 sodium channel impairs embryonic locomotor activities |
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| Authors: | Yau-Hung Chen Fong-Lee Huang Yi-Chuan Cheng Chia-Jung Wu Cheng-Ning Yang Huey-Jen Tsay |
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| Affiliation: | (1) Graduate Institute of Life Sciences, Tamkang University, Taipei, Taiwan;(2) Department of Anatomy, School of Medicine, National Yang-Ming University, Taipei, Taiwan;(3) Department of Biochemistry and Molecular Biology, Chang-Gung University, Taoyuan, Taiwan;(4) Institute of Neuroscience, School of Life Sciences, Brain Research Center, National Yang-Ming University, ROC, No. 155, Sec. 2, Li-Nung Street, Taipei, 112, Taiwan, ROC |
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| Abstract: | Although multiple subtypes of sodium channels are expressed in most neurons, the specific contributions of the individual sodium channels remain to be studied. The role of zebrafish Nav1.6 sodium channels in the embryonic locomotor movements has been investigated by the antisense morpholino (MO) knockdown. MO1 and MO2 are targeted at the regions surrounding the translation start site of zebrafish Nav1.6 mRNA. MO3 is targeted at the RNA splicing donor site of exon 2. The correctly spliced Nav1.6 mRNA of MO3 morphants is 6% relative to that of the wild-type embryos. Nav1.6-targeted MO1, MO2 and MO3 attenuate the spontaneous contraction, tactile sensitivity, and swimming in comparison with a scrambled morpholino and mutated MO3 morpholino. No significant defect is observed in the development of slow muscles, the axonal projection of primary motoneurons, and neuromuscular junctions. The movement impairments caused by MO1, MO2, and MO3 suggest that the function of Nav1.6 sodium channels is essential on the normal early embryonic locomotor activities. |
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| Keywords: | zebrafish sodium channel morpholino locomotor activities |
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