Premium
Decreased acetylcholine receptor content in denervated skeletal muscles infused with nerve extract
Author(s) -
Sayers S.T.,
Yeoh H.C.,
McLane J.A.,
Held I.R.
Publication year - 1986
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490160307
Subject(s) - denervation , acetylcholine receptor , chemistry , skeletal muscle , sciatic nerve , medicine , endocrinology , acetylcholine , in vivo , neuromuscular junction , soleus muscle , receptor , bungarotoxin , motor nerve , biochemistry , anatomy , biology , microbiology and biotechnology , neuroscience
The influence of a concentrated extract of soluble substances from the sciatic nerve upon the acetylcholine receptor (AChR) content in the soleus muscle of adult rats was examined by in vivo infusions. Internal and membrane‐inserted AChR were quantitated by the specific binding of 125 I‐alpha‐bungarotoxin (a‐BuTX). Interestingly, the nerve extract had no apparent effect unless the soleus muscle was also denervated at the start of the infusion. Then, after 66 hr, substantially less (60‐80%) binding of 125 I‐a‐BuTX to AChR was observed compared to denervated solei that did not receive an infusion of nerve extract. However, the concentration of protein in the nerve extract had to exceed 5 mg/ml before this effect was evident. Infusions of phosphate‐buffered saline, bovine serum albumin, rat liver extract, or human transferrin had no striking effect upon AChR. The prevention of the characteristic denervation‐induced increase in nonjunctional AChR by an active component in the nerve extract may be due to a trophic signal for decreased synthesis of AChR, but it is also possible that the degradation of AChR was increased.