The trp gene encodes a plasma membrane channel with close homology to the dihydropyridine receptor.

It is also known as CACNL1A3 and the dihydropyridine receptor (DHPR).

The T-tubule system contains voltage-dependent calcium channels known as dihydropyridine receptors (DHP) which are activated by the end-plate potential.

Rather than releasing calcium from the T-tubules, activated dihydropyridine receptors transmit the voltage-mediated signal through a mechanical linkage to the ryanodine receptors in the sarcoplasmic reticulum.

By contrast in cardiac muscle, ryanodine receptors are activated by the Ca current of activated dihydropyridine receptor Ca channels (see Ca-induced Ca release).

A stimulus, in the form of positively charged current, is transmitted from the neuromuscular junction down the length of the T tubules, activating dihydropyridine receptors (DHPRs).

In skeletal muscle, it is thought that activation occurs via a physical coupling to the dihydropyridine receptor, whereas, in cardiac muscle, the primary mechanism is calcium-induced calcium release from the sarcoplasmic reticulum.

For example, in skeletal muscle, ryanodine receptors are physically linked to surface membrane dihydropyridine receptor Ca channels so that activation of these channels by membrane depolarisation leads to ryanodine receptor activation.

The depolarization activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.

The dihydropyridine receptor in the surface membrane senses a change in voltage (V)and undergoes a conformational change which is transmitted through the bulbous head of the RYR to open the calcium channel in the sarcoplasmic reticulum.