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Author Notes:

David J. Bennett, bennettd@ualberta.ca

K.H, and A.M.L-O. designed the study, carried out the animal experiments and analyzed data. K.M. and M.A.G. designed and performed the human experiments. N.P. and K.E.J. designed and performed the computer simulations. S.L., S.B., A.M., M.J.S. and R.S. assisted with animal electrophysiology. K.F. and A.M.L-O provided confocal microscopy. K.K.F, S.L., D.A.R. and K.H. developed the transgenic mice and performed the optogenetic experiments. R.A.P. developed transgenic mice used in immunohistochemical studies. Y.L. and D.J.B. conceived and designed the study, carried out experiments and analyzed data. D.J.B, K.H., and Y.L. wrote the paper, with editing from other authors. These authors contributed equally: K.H and A.M.L-O. These authors jointly supervised this work as senior authors: Y.L., K.K.F. and D.J.B.

We thank Leo Sanelli, Jennifer Duchcherer, Babak Afsharipour and Christopher K. Thompson for technical assistance, and Shawn Hochman, CJ Heckman, FJ Alvarez and Tia Bennett for discussions and editing the manuscript. VGLUT1Cre mice cords were kindly donated by Dr. FJ Alvarez. We thank Prof Uwe Rudolph (McLean Hospital, currently University of Illinois Urbana-Champaign) for providing Gabra5-floxed mice. This research was supported by the Canadian Institutes of Health Research (MOP 14697 and PJT 165823 D.J.B.) and the US National Institutes of Health (NIH, R01NS47567, D.J.B. and K.F.; R01GM118801, R.A.P.). These funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.

All authors declare no competing interests.



  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • CAT

GABA facilitates spike propagation through branch points of sensory axons in the spinal cord

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Journal Title:



Volume 25, Number 10


, Pages 1288-+

Type of Work:

Article | Post-print: After Peer Review


Movement and posture depend on sensory feedback that is regulated by specialized GABAergic neurons (GAD2+) that form axo-axonic contacts onto myelinated proprioceptive sensory axons and are thought to be inhibitory. However, we report here that activating GAD2+ neurons directly with optogenetics or indirectly by cutaneous stimulation actually facilitates sensory feedback to motor neurons in rodents and humans. GABAA receptors located at or near nodes of Ranvier of sensory axons cause this facilitation by preventing spike propagation failure at the many axon branch points, which is otherwise common without GABA. In contrast, GABAA receptors are generally lacking from axon terminals and so cannot inhibit transmitter release onto motor neurons, unlike GABAB receptors that cause presynaptic inhibition. GABAergic innervation near nodes and branch points allows individual branches to function autonomously, with GAD2+ neurons regulating which branches conduct, adding a computational layer to the neuronal networks generating movement and likely generalizing to other central nervous system axons.
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