ABSTRACT
When the T-tubule membrane is depolarized by a muscle action potential, voltage-sensing proteins known as dihydropyridine receptors (that are embedded in the T-tubule membrane in close apposition to the SR) are acti vated. A chemical or mechanical interaction between the dihydropyridine recep tors and ryanodine receptors (calcium channels present in the SR membrane) allows the flow of calcium ions from the SR into the sarcoplasm via the ryan odine receptor channels, although the exact mechanism for this has yet to be fully elucidated. The muscle action potential that induces this release of calcium ions is short-lived, and after a few milliseconds, the ryanodine receptor channels close and calcium-ATPases mop up the excess calcium ions from the sarcoplasm. The concentrations of calcium ions in the sarcoplasm are >10000fold higher during depolarization of the T-tubule (>10 μM) than when it is normally polarized (<1 nM). It is this change in calcium ion concentration in the sarcoplasm that induces contraction of the muscle fiber (see 'The crossbridge cycle' below).
