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The Journal of Neuroscience, March 2, 2005, 25(9):2226-2232; doi:10.1523/JNEUROSCI.5065-04.2005

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Behavioral/Systems/Cognitive
Regulation of Motoneuron Excitability via Motor Endplate Acetylcholine Receptor Activation

Stan T. Nakanishi,¹ Timothy C. Cope,¹ Mark M. Rich,^1,2 Dario I. Carrasco,¹ and Martin J. Pinter¹

Departments of ¹Physiology and ²Neurology, Emory University School of Medicine, Atlanta, Georgia 30322

Motoneuron populations possess a range of intrinsic excitability that plays an important role in establishing how motor units are recruited. The fact that this range collapses after axotomy and does not recover completely until after reinnervation occurs suggests that muscle innervation is needed to maintain or regulate adult motoneuron excitability, but the nature and identity of underlying mechanisms remain poorly understood. Here, we report the results of experiments in which we studied the effects on rat motoneuron excitability produced by manipulations of neuromuscular transmission and compared these with the effects of peripheral nerve axotomy. Inhibition of acetylcholine release from motor terminals for 5-6 d with botulinum toxin produced relatively minor changes in motoneuron excitability compared with the effect of axotomy. In contrast, the blockade of acetylcholine receptors with -bungarotoxin over the same time interval produced changes in motoneuron excitability that were statistically equivalent to axotomy. Muscle fiber recordings showed that low levels of acetylcholine release persisted at motor terminals after botulinum toxin, but endplate currents were completely blocked for at least several hours after daily intramuscular injections of -bungarotoxin. We conclude that the complete but transient blockade of endplate currents underlies the robust axotomy-like effects of -bungarotoxin on motoneuron excitability, and the low level of acetylcholine release that remains after injections of botulinum toxin inhibits axotomy-like changes in motoneurons. The results suggest the existence of a retrograde signaling mechanism located at the motor endplate that enables expression of adult motoneuron excitability and depends on acetylcholine receptor activation for its normal operation.

Key words: acetylcholine; receptor; transmitter release; motoneuron; excitability; neuromuscular

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Received Dec 13, 2004; revised January 18, 2005; accepted January 18, 2005.

This article has been cited by other articles:

				E. K. Bichler, S. T. Nakanishi, Q.-B. Wang, M. J. Pinter, M. M. Rich, and T. C. Cope Enhanced Transmission at a Spinal Synapse Triggered In Vivo by an Injury Signal Independent of Altered Synaptic Activity J. Neurosci., November 21, 2007; 27(47): 12851 - 12859. [Abstract] [Full Text] [PDF]

				E. K. Bichler, D. I. Carrasco, M. M. Rich, T. C. Cope, and M. J. Pinter Rat motoneuron properties recover following reinnervation in the absence of muscle activity and evoked acetylcholine release J. Physiol., November 15, 2007; 585(1): 47 - 56. [Abstract] [Full Text] [PDF]

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