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 | |
| State | Published - 1991 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle. / Shyng, Show-Ling; Xu, R.; Salpeter, M. M.
In: Neuron, Vol. 6, No. 3, 1991, p. 469-475.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle
AU - Shyng, Show-Ling
AU - Xu, R.
AU - Salpeter, M. M.
PY - 1991
Y1 - 1991
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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U2 - 10.1016/0896-6273(91)90254-W
DO - 10.1016/0896-6273(91)90254-W
M3 - Article
VL - 6
SP - 469
EP - 475
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 3
ER -