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dc.contributor.authorZhang, Hong Yan
dc.contributor.authorPicton, Laurence David
dc.contributor.authorLi, Wen-Chang
dc.contributor.authorSillar, Keith Thomas
dc.identifier.citationZhang , H Y , Picton , L D , Li , W-C & Sillar , K T 2015 , ' Mechanisms underlying the activity-dependent regulation of locomotor network performance by the Na + pump ' , Scientific Reports , vol. 5 , 16188 .
dc.identifier.otherPURE: 223450255
dc.identifier.otherPURE UUID: 92744af1-e37c-451b-846d-2abe06b65177
dc.identifier.otherScopus: 84946867398
dc.identifier.otherWOS: 000364198500001
dc.identifier.otherORCID: /0000-0002-1179-6636/work/64361137
dc.identifier.otherORCID: /0000-0003-0171-3814/work/64393779
dc.descriptionThis research was funded by BBSRC (project grants to KTS (BB/F015488/1) and W-CL; EastBio studentship to LP) and Wellcome Trust (ISSF to H-YZ).en
dc.description.abstractActivity-dependent modification of neural network output usually results from changes in neurotransmitter release and/or membrane conductance. In Xenopus frog tadpoles, spinal locomotor network output is adapted by an ultraslow afterhyperpolarization (usAHP) mediated by an increase in Na+ pump current. Here we systematically explore how the interval between two swimming episodes affects the second episode, which is shorter and slower than the first episode. We find the firing reliability of spinal rhythmic neurons to be lower in the second episode, except for excitatory descending interneurons (dINs). The sodium/proton antiporter, monensin, which potentiates Na+ pump function, induced similar effects to short inter-swim intervals. A usAHP induced by supra-threshold pulses reduced neuronal firing reliability during swimming. It also increased the threshold current for spiking and introduced a delay to the first spike in a train, without reducing subsequent firing frequency. This delay was abolished by ouabain or zero K+ saline, which eliminate the usAHP. We present evidence for an A-type K+ current in spinal CPG neurons which is inactivated by depolarization and de-inactivated by hyperpolarization, and accounts for the prolonged delay. We conclude that the usAHP attenuates neuronal responses to excitatory network inputs by both membrane hyperpolarization and enhanced de-inactivation of an A-current.
dc.relation.ispartofScientific Reportsen
dc.rightsCopyright 2015 the Authors. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
dc.subjectRC0321 Neuroscience. Biological psychiatry. Neuropsychiatryen
dc.titleMechanisms underlying the activity-dependent regulation of locomotor network performance by the Na+ pumpen
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews.School of Psychology and Neuroscienceen
dc.contributor.institutionUniversity of St Andrews.East of Scotland Bioscience Doctoral Training Partnershipen
dc.contributor.institutionUniversity of St Andrews.Institute of Behavioural and Neural Sciencesen
dc.description.statusPeer revieweden

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