The electrophysiological expression of Ca2+ channels and of apamin sensitive Ca2+ activated K+ channels is abolished in skeletal muscle cells from mice with muscular dysgenesis

Romey, Georges; Rieger, François; Renaud, Jean‐François; Pinçon‐Raymond, Martine; Lazdunski, Michel

doi:10.1016/0006-291x(86)90422-5

Cited by 24 publications

(2 citation statements)

References 23 publications

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“…Therefore, birth cannot occur and the disease must be studied at the fetal stage. Skeletal muscles from fetal mdg/mdg mice have been shown to lack receptors for Ca channel effectors (PinconRaymond et al, 1985), as well as functional L-type Ca channels (Beam, Knudson & Powell, 1986;Romey et al, 1986), whereas the number of DHP receptors, as well as Ca channel function, appeared to be normal in cardiac muscle and the central nervous system (Beam et al, 1986;Romey et al, 1986). The disappearance of skeletal muscle Ca channels in the mutant was associated with the absence of the norreal triadic structure which appears to be essential for normal channel expression in skeletal muscle (Pincon-Raymond et al, 1985).…”

Section: Defects In Ca Channels Are Related To Several Pathological Smentioning

confidence: 98%

Calcium channels: Molecular pharmacology, structure and regulation

1988

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Section: Defects In Ca Channels Are Related To Several Pathological Smentioning

confidence: 98%

Calcium channels: Molecular pharmacology, structure and regulation

1988

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“…Identification of the unique population of large particles in junctional domains of the plasmalemma and T tubules with L-type channels (DHPRs) is now well accepted for skeletal and cardiac muscle, where it is based on multiple evidence. In skeletal muscle the particles were identified as DHPRs based on coincidental lack of e-c coupling and of the large particle clusters in dysgenic muscle lacking the ␣1 subunit of DHPRs (Rieger et al, 1987, Tanabe et al, 1988Romey et al, 1986;Franzini-Armstrong et al, 1991) and on reconstitution of e-c coupling and large particle clusters by transfections with cDNA for the DHPR (Tanabe et al, 1988;Takekura et al, 1994). Cardiac muscle particles were later identified as DHPRs based on similarity in size to the skeletal DHPR particles (Sun et al, 1995;Protasi et al, 1997), in addition to the co-localization of RyR and DHPRs at the light microscope level and the proximity of particle patches to foot-bearing SR in electron micrographs (Carl et al, 1995;Sun et al, 1995;Protasi et al, 1997;Gathercole et al., 2000).…”

Section: Discussionmentioning

confidence: 99%

The Structure of Ca2+ Release Units in Arthropod Body Muscle Indicates an Indirect Mechanism for Excitation-Contraction Coupling

Takekura

Franzini‐Armstrong

2002

Biophysical Journal

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The relative disposition of ryanodine receptors (RyRs) and L-type Ca(2+) channels was examined in body muscles from three arthropods. In all muscles the disposition of ryanodine receptors in the junctional gap between apposed SR and T tubule elements is highly ordered. By contrast, the junctional membrane of the T tubule is occupied by distinctive large particles that are clustered within the small junctional domain, but show no order in their arrangement. We propose that the large particles of the junctional T tubules represent L-type Ca(2+) channels involved in excitation-contraction (e-c) coupling, based on their similarity in size and location with the L-type Ca(2+) channels or dihydropyridine receptors (DHPRs) of skeletal and cardiac muscle. The random arrangement of DHPRs in arthropod body muscles indicates that there is no close link between them and RyRs. This matches the architecture of vertebrate cardiac muscle and is in keeping with the similarity in e-c coupling mechanisms in cardiac and invertebrate striated muscles.

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Myotube driven myogenic recruitment of cells during in vitro myogenesis

Breton

Paulin

et al. 1995

Developmental Dynamics

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Muscular dysgenesis (mdg) is a recessive lethal mutation in the mouse which drastically affects skeletal muscle development during embryonic life. Physiologically, the disease is characterized by a complete paralysis resulting from a lack of excitation-contraction coupling. Existing electrophysiological, biochemical, and genetic evidence shows that mdg/mdg mice express a basic alteration of L-type voltage-sensitive Ca2+ channels in skeletal muscle. Studies on mdg/mdg myotubes in primary culture have shown that +/+ fibroblasts or +/+ Schwann cells may fuse with them and correct their functional deficiency by genetic complementation. As the spontaneous formation of heterocaryons is thought to be an exclusive property of myoblasts, we asked whether fibroblasts may have changed their properties before fusion occurred. We used primary cells issued from sciatic nerves dissected from newborn transgenic mice carrying the pHuDes1-nls-LacZ transgene (Des-LacZ cells) as non-muscle cells. These cells were mainly fibroblasts (80%) positive for Thy1.1 and Schwann cells positive for S100. The cultures were negative for myogenic markers (desmin, troponin T), did not form myotubes long-term, and did not display significant activation of the muscle reporter gene (pHuDes1-nls-LacZ). After a few days in coculture with dysgenic or normal myotubes, the muscle reporter gene (beta-galactosidase) was detected both within dysgenic myotubes, correlating with the restoration of normal contractile activity, and normal myotubes. As well as confirming that fusion takes place, this shows that Des-LacZ cells nuclei incorporated into recipient myotubes express their own myogenic genes. Moreover, individual mononucleated Des-LacZ cells expressing beta-galactosidase were observed, indicating that myogenic genes were being expressed before fusion. This suggests a mechanism of myotube driven myogenic recruitment of cells during the in vitro myogenesis. Analysis of the distribution of the induced Des-LacZ cells (positive for beta-galactosidase) in compartmentalized muscle cocultures showed that in the presence of dysgenic myotubes, these cells were equally distributed in both myotube free and enriched areas, whereas in the presence of normal myotubes, the positive cells remained in close vicinity of the myotubes. This difference could be explained by the fact that the dysgenic phenotype might include release of the induction process from its normal controls. Our results are consistent with the idea of a transcellular mechanism triggering myogenic differentiation in non-muscle cells, and that myotubes themselves are able to drive myogenic recruitment of cells during the in vitro myogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

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The electrophysiological expression of Ca2+ channels and of apamin sensitive Ca2+ activated K+ channels is abolished in skeletal muscle cells from mice with muscular dysgenesis

Cited by 24 publications

References 23 publications

Calcium channels: Molecular pharmacology, structure and regulation

Calcium channels: Molecular pharmacology, structure and regulation

The Structure of Ca2+ Release Units in Arthropod Body Muscle Indicates an Indirect Mechanism for Excitation-Contraction Coupling

Myotube driven myogenic recruitment of cells during in vitro myogenesis

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