Dihydropyridine receptor (DHPR) is a surface membrane protein critical for
the excitation-contraction coupling of striated muscle. DHPR and the sarcoplasmic
reticulum ryanodine receptor (RyR) are two key components of the
intracellular junctions, where depolarization of the surface membrane is converted
into the release of Ca2+ from internal stores. The α1-subunit of the
DHPR contains a cytoplasmic loop which is thought to be involved in the interactions
with RyR. Phosphorylation of the DHPR α1-subunit is also thought to
play a role in the functional interaction of DHPR and RyR. Mutation in DHPR
α1 results in excitation-contraction uncoupling, leading to muscular dysgenesis,
a complete inactivity in developing skeletal muscles. Cells that do not
express RyR also lack excitation-contraction coupling and exhibit a severalfold
reduction in Ca2+ current density.