TY - JOUR
T1 - Effect of reinnervation on the degradation rate of junctional acetylcholine receptors synthesized in denervated skeletal muscles
AU - Shyng, S. L.
AU - Salpeter, M. M.
PY - 1990
Y1 - 1990
N2 - Two populations of ACh receptors (AChRs) with different degradation rates have been shown to coexist in the postsynaptic membrane after denervation of the neuromuscular junction (NMJ). One population, consisting of the slowly degrading original AChRs inserted into the plasma membrane prior to denervation, has a degradation half-life (t1/2) of ∼8 d. This degradation rate accelerates after denervation (to a t1/2 ∼ 3 d), but can be decelerated back to the predenervation rate by reinnervation. The second population, the rapidly degrading new AChRs, which replace the degrading original AChRs at the NMJ after denervation, resembles embryonic AChRs, with a t1/2 of ∼ 1 d. In the present study, we report that the degradation rate of these new junctional AChRs is unaltered for 3-6 half-lives after reinnervation. We further report that a small amount (<10%) of slowly degrading AChRs (t1/2 ∼ 3 d) may also be synthesized in denervated muscle. We suggest that, unlike its effect on the original, slowly degrading AChRs, reinnervation does not modulate the degradation rate of the rapidly degrading new junctional AChRs. It merely regulates the ratio of rapidly to slowly degrading AChRs being synthesized and inserted at the NMJ.
AB - Two populations of ACh receptors (AChRs) with different degradation rates have been shown to coexist in the postsynaptic membrane after denervation of the neuromuscular junction (NMJ). One population, consisting of the slowly degrading original AChRs inserted into the plasma membrane prior to denervation, has a degradation half-life (t1/2) of ∼8 d. This degradation rate accelerates after denervation (to a t1/2 ∼ 3 d), but can be decelerated back to the predenervation rate by reinnervation. The second population, the rapidly degrading new AChRs, which replace the degrading original AChRs at the NMJ after denervation, resembles embryonic AChRs, with a t1/2 of ∼ 1 d. In the present study, we report that the degradation rate of these new junctional AChRs is unaltered for 3-6 half-lives after reinnervation. We further report that a small amount (<10%) of slowly degrading AChRs (t1/2 ∼ 3 d) may also be synthesized in denervated muscle. We suggest that, unlike its effect on the original, slowly degrading AChRs, reinnervation does not modulate the degradation rate of the rapidly degrading new junctional AChRs. It merely regulates the ratio of rapidly to slowly degrading AChRs being synthesized and inserted at the NMJ.
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U2 - 10.1523/jneurosci.10-12-03905.1990
DO - 10.1523/jneurosci.10-12-03905.1990
M3 - Article
C2 - 2269890
AN - SCOPUS:0025582538
SN - 0270-6474
VL - 10
SP - 3905
EP - 3915
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 12
ER -