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This Article Full Text Full Text (PDF) All Versions of this Article: 585/1/47    most recent jphysiol.2007.135541v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bichler, E. K. Articles by Pinter, M. J. Search for Related Content PubMed PubMed Citation Articles by Bichler, E. K. Articles by Pinter, M. J. Related Collections Neuroscience

¹ Department Physiology, Emory University, Atlanta, GA, USA
² Department Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH, USA

Available evidence supports the idea that muscle fibres provide retrograde signals that enable the expression of adult motoneuron electrical properties but the mechanisms remain unknown. We showed recently that when acetylcholine receptors are blocked at motor endplates, the electrical properties of rat motoneurons change in a way that resembles changes observed after axotomy. This observation suggests that receptor blockade and axotomy interrupt the same signalling mechanisms but leaves open the possibility that the loss of muscle fibre activity underlies the observed effects. To address this issue, we examined the electrical properties of axotomized motoneurons following reinnervation. Ordinarily, these properties return to normal following reinnervation and re-activation of muscle, but in this study muscle fibre activity and evoked acetylcholine release were prevented during reinnervation by blocking axonal conduction. Under these conditions, the properties of motoneurons that successfully reinnervated muscle fibres recovered to normal despite the absence of muscle fibre activity and evoked release. We conclude that the expression of motoneuron electrical properties is not regulated by muscle fibre activity but rather by a retrograde signalling system coupled to activation of endplate acetylcholine receptors. Our results indicate that spontaneous release of acetylcholine from regenerated motor terminals is sufficient to operate the system.

(Received 30 April 2007; accepted after revision 16 September 2007; first published online 20 September 2007)
Corresponding author M. J. Pinter: Department of Physiology, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, USA. Email: mpinter{at}physio.emory.edu