| First Author | Nakai J | Year | 1996 |
| Journal | Nature | Volume | 380 |
| Issue | 6569 | Pages | 72-5 |
| PubMed ID | 8598910 | Mgi Jnum | J:119621 |
| Mgi Id | MGI:3702850 | Doi | 10.1038/380072a0 |
| Citation | Nakai J, et al. (1996) Enhanced dihydropyridine receptor channel activity in the presence of ryanodine receptor. Nature 380(6569):72-5 |
| abstractText | Excitation-contraction coupling in skeletal muscle involves a voltage sensor in the plasma membrane which, in response to depolarization, causes an intracellular calcium-release channel to open. The skeletal isoform of the ryanodine receptor (RyR-1) functions as the Ca2+-release channel and the dihydropyridine receptor (DHPR) functions as the voltage sensor and also as an L-type Ca2+ channel. Here we examine the possibility that there is a retrograde signal from RyR-1 to the DHPR, using myotubes from mice homozygous for a disrupted RyR-1 gene (dyspedic mice). As expected, we find that there is no excitation-contraction coupling in dyspedic myotubes, but we also find that they have a roughly 30-fold reduction in L-type Ca2+-current density. Injection of dyspedic myotubes with RyR-1 complementary DNA restores excitation-contraction coupling and causes the density of L-type Ca2+ current to rise towards normal. Despite the differences in Ca2+-current magnitude, measurements of charge movement indicate that the density of DHPRs is similar in dyspedic and RyR-1-expressing myotubes. Our results support the possibility of a retrograde signal by which RyR-1 enhances the function of DHPRs as Ca2+ channels. |
