Abstract
Muscle fibers release large amounts of calcium from an internal compartment,
the sarcoplasmic reticulum (SR), during activation. Two proteins
are involved in this process and its control: plasma membrane calcium
channels, or dihydropyridine receptors (DHPRs), and SR calcium release
channels, or ryanodine receptors (RyRs). The two proteins form part
of a structural complex, perhaps unique to muscle cells, which allows
an interaction between plasma membrane and SR, resulting in calcium
release from the latter. The surface-SR interaction is a step in
the coupling between electrical events in the plasma membrane and
contraction (excitation-contraction coupling). The structural complexes
have been called calcium release units. One key to further understanding
the control of calcium homeostasis in muscle is knowledge of how
DHPRs and RyRs assemble into calcium release units. We have studied
the development of avian myocardium, using immunocytochemistry to
locate DHPRs and RyRs and electron microscopy to follow the formation
of calcium release units containing feet (RyRs) and large membrane
particles (presumably DHPRs). We find that the initial step is a
docking of SR vesicles to the plasma membrane, followed by the appearance
of feet in the junctional gap between SR and plasma membrane. Feet
aggregate in ordered arrays, and the arrays increase in size until
they fill the entire junctional gap. Clustering of membrane particles,
presumably DHPRs, is apparently coupled to clustering of feet, since
the two junction components assemble within patches of membrane of
approximately equal size and containing an approximately constant
ratio of particles to feet. Thus, despite the fact that no evidence
exists for a direct interaction between DHPRs and RyRs in cardiac
muscle, some mechanism exists to ensure that the two molecules are
clustered in proximity to each other and in the appropriate proportion.
Description
The whole bibliography file I use.
Links and resources
Tags