Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle

S. L. Shyng; R. Xu; M. M. Salpeter

doi:10.1016/0896-6273(91)90254-W

Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle

S. L. Shyng
, R. Xu
, M. M. Salpeter

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

Abstract

We used mouse diaphragm muscle in organ culture to study the stabilization of acetylcholine receptor (AChR) degradation at denervated neuromuscular junctions. After denervation, the degradation rate of the AChRs present prior to denervation (slowly degrading, or Rs, AChRs) accelerates from the predenervation degradation half-life (t_{1 2}) of ∼8-10 days to a t_{1 2} of ∼2-3 days. We report that addition to the organ culture medium of pharmacological agents that elevate cytoplasmic cAMP levels (forskolin, dibutyryl cAMP, and 8-bromo-cAMP) reversed the change in 42 caused by denervation, whereas addition of 1,9-dideoxyforskolin, a forskolin analog that does not elevate cytoplasmic cAMP levels, did not reverse the effect of denervation. The degradation rate of AChRs in primary myotube cultures and that of the newly synthesized AChRs in denervated muscle were little affected by forskolin or dibutyryl cAMP. The possibility is raised that the modulation of Its AChR degradation by innervation may be mediated by CAMP.

Original language	English (US)
Pages (from-to)	469-475
Number of pages	7
Journal	Neuron
Volume	6
Issue number	3
DOIs	https://doi.org/10.1016/0896-6273(91)90254-W
State	Published - Mar 1991
Externally published	Yes

Funding

We thank Daniel Wetzel, Dorothy Bell, and Iris Greenberg for assistance with these experiments, Tom Podleski and Ron Harris-Warrick for helpful discussion, and Deborah Moslehi for preparing the manuscript. This work was supported by grants from the National Institutes of Health (NS09315) and from the Cornell University Biotechnology Program sponsored by the N.Y. State Science and Technology Foundation, by a consortium of industries, and by the United States Army Research Office and NSF.

Funders	Funder number
N.Y. State Science and Technology Foundation
United States Army Research Office
Author National Science Foundation National Science Foundation National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health National Science Foundation National Science Foundation
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	NS09315

ASJC Scopus subject areas

General Neuroscience

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10.1016/0896-6273(91)90254-W

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title = "Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle",

abstract = "We used mouse diaphragm muscle in organ culture to study the stabilization of acetylcholine receptor (AChR) degradation at denervated neuromuscular junctions. After denervation, the degradation rate of the AChRs present prior to denervation (slowly degrading, or Rs, AChRs) accelerates from the predenervation degradation half-life (t 1 2) of ∼8-10 days to a t 1 2 of ∼2-3 days. We report that addition to the organ culture medium of pharmacological agents that elevate cytoplasmic cAMP levels (forskolin, dibutyryl cAMP, and 8-bromo-cAMP) reversed the change in 42 caused by denervation, whereas addition of 1,9-dideoxyforskolin, a forskolin analog that does not elevate cytoplasmic cAMP levels, did not reverse the effect of denervation. The degradation rate of AChRs in primary myotube cultures and that of the newly synthesized AChRs in denervated muscle were little affected by forskolin or dibutyryl cAMP. The possibility is raised that the modulation of Its AChR degradation by innervation may be mediated by CAMP.",

author = "Shyng, \{S. L.\} and R. Xu and Salpeter, \{M. M.\}",

note = "Funding Information: We thank Daniel Wetzel, Dorothy Bell, and Iris Greenberg for assistance with these experiments, Tom Podleski and Ron Harris-Warrick for helpful discussion, and Deborah Moslehi for preparing the manuscript. This work was supported by grants from the National Institutes of Health (NS09315) and from the Cornell University Biotechnology Program sponsored by the N.Y. State Science and Technology Foundation, by a consortium of industries, and by the United States Army Research Office and NSF.",

year = "1991",

month = mar,

doi = "10.1016/0896-6273(91)90254-W",

language = "English (US)",

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journal = "Neuron",

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AU - Xu, R.

AU - Salpeter, M. M.

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PY - 1991/3

Y1 - 1991/3

N2 - We used mouse diaphragm muscle in organ culture to study the stabilization of acetylcholine receptor (AChR) degradation at denervated neuromuscular junctions. After denervation, the degradation rate of the AChRs present prior to denervation (slowly degrading, or Rs, AChRs) accelerates from the predenervation degradation half-life (t 1 2) of ∼8-10 days to a t 1 2 of ∼2-3 days. We report that addition to the organ culture medium of pharmacological agents that elevate cytoplasmic cAMP levels (forskolin, dibutyryl cAMP, and 8-bromo-cAMP) reversed the change in 42 caused by denervation, whereas addition of 1,9-dideoxyforskolin, a forskolin analog that does not elevate cytoplasmic cAMP levels, did not reverse the effect of denervation. The degradation rate of AChRs in primary myotube cultures and that of the newly synthesized AChRs in denervated muscle were little affected by forskolin or dibutyryl cAMP. The possibility is raised that the modulation of Its AChR degradation by innervation may be mediated by CAMP.

AB - We used mouse diaphragm muscle in organ culture to study the stabilization of acetylcholine receptor (AChR) degradation at denervated neuromuscular junctions. After denervation, the degradation rate of the AChRs present prior to denervation (slowly degrading, or Rs, AChRs) accelerates from the predenervation degradation half-life (t 1 2) of ∼8-10 days to a t 1 2 of ∼2-3 days. We report that addition to the organ culture medium of pharmacological agents that elevate cytoplasmic cAMP levels (forskolin, dibutyryl cAMP, and 8-bromo-cAMP) reversed the change in 42 caused by denervation, whereas addition of 1,9-dideoxyforskolin, a forskolin analog that does not elevate cytoplasmic cAMP levels, did not reverse the effect of denervation. The degradation rate of AChRs in primary myotube cultures and that of the newly synthesized AChRs in denervated muscle were little affected by forskolin or dibutyryl cAMP. The possibility is raised that the modulation of Its AChR degradation by innervation may be mediated by CAMP.

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Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle

Abstract

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ASJC Scopus subject areas

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