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Building Finite Element Models to Investigate Zebrafish Jaw Biomechanics
Published on: December 3, 2016
Neuromuscular remodeling and myofiber turnover in Rana pipiens' jaw muscles
1Departments of Oral Biology, Cell Biology, Neurobiology and Anatomy, Ohio State University, Columbus 43210, USA. alley.2@osu.edu
Abstract:
Larval jaw myofibers in Rana pipiens degenerate during metamorphosis and are replaced by a second wave of myogenesis that provides for adult jaw function. Trigeminal motoneurons that innervate larval myofibers transfer their preterminal axons to these adult successors where they establish new motor endplates. Silver/acetyl-cholinesterase histochemistry was used to compare innervation patterns in the larval and adult jaw adductor muscles and to plot the time course over which these changes occur. Innervation patterns differ substantially on the pre- and postmetamorphic myofiber populations. Jaw myofibers in the tadpole were unique by virtue of their exceedingly high level of distributed and focal polyinnervation. Each myofiber was innervated by approximately 10 small, junctional zones, most containing multiple axons, diffusely distributed over the length excepting small junctional free zones at either end of the muscle. In juvenile frogs, immediately following redeployment, the replacement myofibers had a polyinnervation pattern that mirrors that observed in the larvae. However, by 12 weeks after metamorphosis there was a clear condensation of the end plates into multiple zones. Moreover, jaw myofibers in adult frogs had a reduced level of distributed and focal polyinnervation, less than 15% show signs of polyinnervation. The pattern of polyinnervation, axonal redeployment and myofiber degeneration is consistent with the hypothesis that the larval jaw muscles serve as a population of primary myofibers, ensuring survival of the trigeminal motoneurons through the prolonged period of larval development, while also providing a scaffold on which secondary jaw myofibers are constructed.
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When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.