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The Journal of Neuroscience, August 30, 2006, 26(35):8983-8987; doi:10.1523/JNEUROSCI.2493-06.2006

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Development/Plasticity/Repair
Prolongation of Evoked and Spontaneous Synaptic Currents at the Neuromuscular Junction after Activity Blockade Is Caused by the Upregulation of Fetal Acetylcholine Receptors

Xueyong Wang,¹ Kathrin L. Engisch,¹ Russell W. Teichert,² Baldomero M. Olivera,² Martin J. Pinter,³ and Mark M. Rich¹

¹Department of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, ²Department of Biology, University of Utah, Salt Lake City, Utah 84112, and ³Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322

Correspondence should be addressed to Dr. Mark M. Rich, Room 014, M & M Building, Wright State University, 3640 Colonel Glenn, Dayton, OH 45435. Email: mark.rich{at}wright.edu

It has been shown previously in a number of systems that after an extended block of activity, synaptic strength is increased. We found that an extended block of synaptic activity at the mouse neuromuscular junction, using a tetrodotoxin cuff in vivo, increased synaptic strength by prolonging the evoked endplate current (EPC) decay. Prolongation of EPC decay was accompanied by only modest prolongation of spontaneous miniature EPC (MEPC) decay. Prolongation of EPC decay was reversed when quantal content was lowered by reducing extracellular calcium. These findings suggested that the cause of EPC prolongation was presynaptic in origin. However, when we acutely inhibited fetal-type acetylcholine receptors (AChRs) using a novel peptide toxin (A-conotoxin OIVA[K15N]), prolongation of both EPC and MEPC decay were reversed. We also blocked synaptic activity in a mutant strain of mice in which persistent muscle activity prevents upregulation of fetal-type AChRs. In these mice, there was no prolongation of EPC decay. We conclude that upregulation of fetal-type AChRs after blocking synaptic activity causes modest prolongation of MEPC decay that is accompanied by much greater prolongation of EPC decay. This might occur if acetylcholine escapes from endplates and binds to extrajunctional fetal-type AChRs only during large, evoked EPCs. Our study is the first to demonstrate a functional role for upregulation of extrajunctional AChRs.

Key words: neurotransmitter; synaptic; plasticity; activity; extrajunctional; acetylcholine receptors; transmission; homeostatic; endplate; TTX

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Received June 13, 2006; revised July 21, 2006; accepted July 22, 2006.

Correspondence should be addressed to Dr. Mark M. Rich, Room 014, M & M Building, Wright State University, 3640 Colonel Glenn, Dayton, OH 45435. Email: mark.rich{at}wright.edu

This article has been cited by other articles:

				L. Kong, X. Wang, D. W. Choe, M. Polley, B. G. Burnett, M. Bosch-Marce, J. W. Griffin, M. M. Rich, and C. J. Sumner Impaired Synaptic Vesicle Release and Immaturity of Neuromuscular Junctions in Spinal Muscular Atrophy Mice J. Neurosci., January 21, 2009; 29(3): 842 - 851. [Abstract] [Full Text] [PDF]

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