Biochemical evidence for a complex involving dihydropyridine receptor and ryanodine receptor in triad junctions of skeletal muscle.

Abstract

Membrane vesicles enriched in both ryanodine receptor and dihydropyridine receptor were obtained from rabbit skeletal muscle and solubilized with 3- [(3-cholamidopropyl) (14,17,18).Three different mechanisms have been proposed for excitation-contraction coupling in skeletal muscle: Ca2 -induced Ca2+ release, inositol 1,4,5-trisphosphate-induced Ca2W release, and direct physical coupling (for review see refs. 19 and 20). Current evidence favors a model in which a voltagedriven conformational change ofthe al subunit ofthe DHP-R activates Ca2+ release by the RyR through direct physical interaction (11,21,22

Intracellular Calcium Waves Accompany Neutrophil Polarization, Formylmethionylleucylphenylalanine Stimulation, and Phagocytosis: A High Speed Microscopy Study

“…Thus, we suggest that a strand of the ER mediates the line of communication indicated by the present study. Although we have not studied the mechanism of Ca 2ϩ signal migration from cell surfaces to intracellular membranes, a direct coupling between the L-type Ca 2ϩ channels of the plasma membrane and ryanodine receptors on internal ER membranes is a possibility (51,52), given that we have preliminary evidence suggesting the presence of L-type channels on neutrophils (our unpublished observations). The characteristics of the assembly and regulation of this signaling conduit in living cells will likely contribute to a molecular understanding of why certain receptors do not promote phagolysosome fusion and certain microorganisms escape phagolysosomal destruction.…”

ortho-Substituted Polychlorinated Biphenyls Alter Microsomal Calcium Transport by Direct Interaction with Ryanodine Receptors of Mammalian Brain

“…6, compare traces a, b, and e). 3 to cerebellar microsomes, although higher concentrations did produce a statistically significant enhancement of occupancy that was not seen with coplanar PCB 126 (Fig. 7).…”

“…Fig. 5 illustrates the ability of D-IP 3 to stereoselectively activate IP 3 Rs in the microsomal preparation, since L-IP 3 is inactive (trace a). Addition of 500 M ryanodine to the preparation caused a biphasic response similar to that seen with junctional SR vesicles isolated from striated muscle (31): initially activating and subsequently inactivating RyRs, resulting in net reuptake of the Ca 2ϩ into the cortical vesicles (Fig.…”

“…RyR). Because of structural homologies shared by IP 3 Rs and RyRs, it is necessary to determine if ortho-substituted PCBs discriminate between these microsomal Ca 2ϩ release channels. In neurons, the ryanodine-sensitive stores have thus far been found mainly localized in cell soma, whereas the IP 3 -sensitive stores appear to be equally distributed in neuronal soma and processes (34,35).…”

“…2,3,7, binds to the receptor with the highest affinity and confers the highest potency to induce certain toxic responses, such as wasting syndrome, immunosuppression, and teratogenicity. PCB congeners without ortho-chlorine substitutions are able to confer the coplanar structure similar to TCDD and elicit similar toxicity.…”