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Published online on February 7, 2007, 10.1073/pnas.0611134104
PNAS | February 13, 2007 | vol. 104 | no. 7 | 2448-2453
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BIOLOGICAL SCIENCES / NEUROSCIENCE
Spinal cholinergic interneurons regulate the excitability of motoneurons during locomotion

Gareth B. Miles*, Robert Hartley{dagger}, Andrew J. Todd{dagger}, and Robert M. Brownstone*,{ddagger},§

*Department of Anatomy and Neurobiology, {ddagger}Department of Surgery (Neurosurgery), Dalhousie University, Halifax, NS, Canada B3H 1X5; and {dagger}Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom

Communicated by Thomas M. Jessell, Columbia University Medical Center, New York, NY, December 18, 2006 (received for review July 3, 2006)

To effect movement, motoneurons must respond appropriately to motor commands. Their responsiveness to these inputs, or excitability, is regulated by neuromodulators. Possible sources of modulation include the abundant cholinergic "C boutons" that surround motoneuron somata. In the present study, recordings from motoneurons in spinal cord slices demonstrated that cholinergic activation of m2-type muscarinic receptors increases excitability by reducing the action potential afterhyperpolarization. Analyses of isolated spinal cord preparations in which fictive locomotion was elicited demonstrated that endogenous cholinergic inputs increase motoneuron excitability during locomotion. Anatomical data indicate that C boutons originate from a discrete group of interneurons lateral to the central canal, the medial partition neurons. These results highlight a unique component of spinal motor networks that is critical in ensuring that sufficient output is generated by motoneurons to drive motor behavior.

afterhyperpolarization | C bouton | central pattern generator | muscarinic receptors | spinal cord

Freely available online through the PNAS open access option.

Author contributions: G.B.M., A.J.T., and R.M.B. designed research; G.B.M. and R.H. performed research; G.B.M., R.H., and A.J.T. analyzed data; and G.B.M., A.J.T., and R.M.B. wrote the paper.

The authors declare no conflict of interest.

This article contains supporting information online at www.pnas.org/cgi/content/full/0611134104/DC1.

§To whom correspondence should be addressed at: Department of Anatomy and Neurobiology, Faculty of Medicine, Sir Charles Tupper Medical Building, 14A-5850 College Street, Halifax, NS, Canada B3H 1X5. E-mail: rob.brownstone{at}dal.ca

© 2007 by The National Academy of Sciences of the USA


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