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© The Rockefeller University Press, 0021-9525/1997//159 $5.00
The Journal of Cell Biology, Volume 138, Number 1, , 1997 159-165

Article

Stabilization of Acetylcholine Receptors by Exogenous ATP and Its Reversal by cAMP and Calcium



James P. O'Malley, Charlotte T. Moore, and Miriam M. Salpeter

Section of Neurobiology and Behavior, Cornell University, Ithaca, New York

Innervation of the neuromuscular junction (nmj) affects the stability of acetylcholine receptors (AChRs). A neural factor that could affect AChR stabilization was studied using cultured muscle cells since they express two distinct populations of AChRs similar to those seen at the nmjs of denervated muscle. These two AChR populations are (in a ratio of 9 to 1) a rapidly degrading population (Rr) with a degradation half-life of ~1 d and a slowly degrading population (Rs) that can alternate between an accelerated form (half-life ~3–5 d) and a stabilized form (half-life ~10 d), depending upon the state of innervation of the muscle.

Previous studies have shown that elevation of intracellular cAMP can stabilize the Rs, but not the Rr. We report here that in cultured rat muscle cells, exogenous ATP stabilized the degradation half-life of Rr and possibly also the Rs. Furthermore, pretreatment with ATP caused more stable AChRs to be inserted into the muscle membrane. Thus, in the presence of ATP, the degradation rates of the Rr and Rs overlap. This suggests that ATP released from the nerve may play an important role in the regulation of AChR degradation. Treatment with either the cAMP analogue dibutyryl-cAMP (dB-cAMP) or the calcium mobilizer ryanodine caused the ATP-stabilized Rr to accelerate back to a half-life of 1 d. Thus, at least three signaling systems (intracellular cAMP, Ca2+, and extracellular ATP) have the potential to interact with each other in the building of an adult neuromuscular junction.

1. Abbreviations used in this paper: {alpha}-BTX, {alpha}-bungarotoxin; AChR, acetylcholine receptor; dB-cAMP, dibutyryl cAMP; nmj, neuromuscular junction; PLA2, phospholipase A2; Rr, rapidly degrading acetylcholine receptors; Rs, slowly degrading acetylcholine receptors.

Address all correspondence to Miriam M. Salpeter, Section of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853. Tel.: (607) 254-4341. Fax: (607) 254-4308.

James P. O'Malley' s current address is Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, PA.


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