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Intracellular signaling molecules involved in an inhibitory factor-induced decrease in fetal-type AChR expression.

J M Montgomery1, G Corfas, R G Mills

  • 1Department of Physiology, School of Medical Sciences, and Centre for Neurosciences, Otago University, PO Box 913, Dunedin, New Zealand.

Journal of Neurobiology
|January 20, 2000
PubMed
Summary
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Neural factors, not just muscle activity, reduce fetal acetylcholine receptors (AChRs) in developing muscles. This study identifies protein kinase C and p70(S6k) as key intracellular signals involved in this neurotrophic down-regulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Muscle Physiology

Background:

  • Innervation typically down-regulates fetal acetylcholine receptor (AChR) expression in developing muscle fibers, primarily attributed to muscle activity.
  • Emerging evidence suggests a neural trophic factor also plays a role in this receptor down-regulation.

Purpose of the Study:

  • To investigate the intracellular signaling molecules involved in neurotrophic down-regulation of fetal-type AChR expression.
  • To determine if neural extracts contain a factor responsible for this inhibitory neurotrophic influence.

Main Methods:

  • Utilized skeletal muscle cell lines to assess the effects of neural extracts on fetal-type AChR expression.
  • Investigated the role of intracellular signaling pathways, including protein kinase C and p70(S6k).

Related Experiment Videos

  • Examined the independence of this down-regulation from myogenin and neuregulin.

    • Main Results:

    • Activation of protein kinase C and p70(S6k) was found to be important for AChR down-regulation.
    • The observed decreases in AChR density were independent of myogenin.
    • Receptor down-regulation was also independent of neuregulin, even though neuregulin activates p70(S6k).

    Conclusions:

    • Neural extracts contain an inhibitory factor that down-regulates fetal-type AChR expression.
    • This down-regulation occurs independently of nerve-evoked muscle activity.
    • The process involves intracellular signaling molecules known to regulate AChR expression, specifically protein kinase C and p70(S6k).