Motoneurons regulate the central pattern generator during drug-induced locomotor-like activity in the neonatal mouse

Melanie Falgairolle, Joshua G. Puhl, Avinash Pujala, Wenfang Liu, Michael J. O’Donovan

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

Abstract

Motoneurons are traditionally viewed as the output of the spinal cord that do not influence locomotor rhythmogenesis. We assessed the role of motoneuron firing during ongoing locomotor-like activity in neonatal mice expressing archaerhopsin-3 (Arch), halorhodopsin (eNpHR), or channelrhodopsin-2 (ChR2) in Choline acetyltransferase neurons (ChAT+) or Arch in LIM-homeodomain transcription factor Isl1+ neurons. Illumination of the lumbar cord in mice expressing eNpHR or Arch in ChAT+ or Isl1+ neurons, depressed motoneuron discharge, transiently decreased the frequency, and perturbed the phasing of the locomotor-like rhythm. When the light was turned off motoneuron firing and locomotor frequency both transiently increased. These effects were not due to cholinergic neurotransmission, persisted during partial blockade of gap junctions and were mediated, in part, by AMPAergic transmission. In spinal cords expressing ChR2, illumination increased motoneuron discharge and transiently accelerated the rhythm. We conclude that motoneurons provide feedback to the central pattern generator (CPG) during drug-induced locomotor-like activity.

Original languageEnglish (US)
Article numbere26622
JournaleLife
Volume6
DOIs
StatePublished - Jul 3 2017
Externally publishedYes

Bibliographical note

Funding Information:
The authors thank the intramural program of NINDS for financial support. Funding Funder Grant reference number Author National Institutes of Health NINDS Intramural program Melanie Falgairolle Joshua G Puhl Avinash Pujala Wenfang Liu Michael J O’Donovan National Institutes of Health NINDS Intramural NRSA Joshua G Puhl The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Publisher Copyright:
© 2017, eLife Sciences Publications Ltd. All rights reserved.

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