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Related Experiment Videos

Neonatal denervation inhibits the normal postnatal decrease in endplate channel open time.

S M Schuetze, S Vicini

    The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
    |September 1, 1984
    PubMed
    Summary
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    Neural signals regulate acetylcholine receptor (AChR) channel gating during muscle development. Early denervation delays the developmental decrease in AChR channel open time, suggesting innervation is crucial for this process.

    Area of Science:

    • Neuroscience
    • Developmental Biology
    • Muscle Physiology

    Background:

    • Acetylcholine receptors (AChRs) at skeletal muscle endplates undergo significant changes in channel open time (tau) during development.
    • Specifically, apparent mean channel open time decreases over 3-fold between postnatal days 8 and 18 in rat soleus muscles.

    Purpose of the Study:

    • To investigate the role of muscle innervation in the developmental regulation of AChR channel open time.
    • To determine if neural signals influence AChR channel gating beyond the neuromuscular junction.

    Main Methods:

    • Neonatal rat soleus muscles were denervated before the developmental conversion of AChR channel open times.
    • Fluctuation analysis was used to assay tau at denervated endplates between postnatal days 8 and 18.

    Related Experiment Videos

  • Comparison of junctional and extrajunctional AChR apparent open times in innervated fibers.

    • Main Results:

    • Early denervation blocked or significantly delayed the developmental decrease in AChR channel open time.
    • Enhanced extrajunctional acetylcholine sensitivity was observed in muscles contralateral to denervated ones.
    • Apparent open times of extrajunctional AChRs decreased in parallel with endplate AChRs in developing muscles.

    Conclusions:

    • Muscle innervation plays a critical role in regulating the developmental changes in AChR channel gating.
    • Neural regulation of AChR channel properties extends significantly beyond the neuromuscular junction, affecting extrajunctional receptors.