Aggregation Of Myonuclei And The Spread Of Slow-tonic Myosin Immunoreactivity In Developing Muscle-spindles

Aggregation Of Myonuclei And The Spread Of Slow-tonic Myosin Immunoreactivity In Developing Muscle-spindles

Kucera J; Walro J M

Histochemistry

1991

1991

The pattern of regional expression of a slowtonic myosin heavy chain (MHC) isoform was studied in developing rat soleus intrafusal muscle fibers. Binding of the slow-tonic antibody (ATO) began at the equator of prenatal intrafusal fibers where sensory nerve endings are located, and spread into the polar regions of nuclear bag2 and bag1 fibers but not nuclear chain fibers during ontogeny. The onset of the ATO reactivity coincided with the appearance of equatorial clusters of myonuclei (nuclear bag formations) in bag1 and bag2 fibers. Moreover, the intensity of the ATO reaction was strongest in the region of equatorial myonuclei and decreased with increasing distance from the equator of bag1 and bag2 fibers at all stages of prenatal and postnatal development. The polar expansion of ATO reactivity continued throughout the postnatal development of bag1 fibers, but ceased shortly after birth in bag2 fiber coincident with innervation by motor axons. Thus, afferents that innervate the equator might induce the slow-tonic MHC isoform in bag2 and bag1 fibers by regulating the myosin gene expression by equatorial myonuclei, and efferents or twitch contractile activity might inhibit the spread of the slow-tonic MHC isoform into the poles of bag2 but not bag1 fibers. Absence of ATO binding in chain fibers suggests that chain myotubes may not be as susceptible to the effect of afferents as are myotubes that develop into bag2 and bag1 fibers. The different patterns of slow-tonic MHC expression in the three types of intrafusal fiber may therefore result from the interaction of three elements: sensory neurons, motor neurons, and intrafusal myotubes.

Cell Biology; expression; fibers; heavy-chain isoforms; innervation; motor; rat; skeletal-muscle

Journal Article or Conference Abstract Publication

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

381-390

5

96