Functional and Morphological Features of Skeletal Muscle from Mutant Mice Lacking Both Type 1 and Type 3 Ryanodine Receptors

Ikemoto, Takaaki; Komazaki, Shinji; Takeshima, Hiroshi; Nishi, Miyuki; Noda, Tetsuo; Iino, Masamitsu; Endo, Makoto

doi:10.1111/j.1469-7793.1997.305bn.x

Cited by 61 publications

(50 citation statements)

References 21 publications

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“…Mice lacking both RyR1 and RyR3 were also generated. These double-mutant mice did not actively move after birth and died, most probably from respiratory failure, as was the case for RyR1-deficient mice (Ikemoto et al 1997) RyRs are distributed not only in the central nervous system but also at a peripheral level. RyRs are present in the skeletal and cardiac muscle where their activation represents a crucial step for muscle contraction (Rossi and Sorrentino 2002).…”

Section: Discussionmentioning

confidence: 99%

Different involvement of type 1, 2, and 3 ryanodine receptors in memory processes

Galeotti¹,

Quattrone²,

Vivoli³

et al. 2008

Learn. Mem.

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The administration of the ryanodine receptor (RyR) agonist 4-Cmc (0.003-9 nmol per mouse intracerebroventricularly [i.c.v.]) ameliorated memory functions, whereas the RyR antagonist ryanodine (0.0001-1 nmol per mouse i.c.v.) induced amnesia in the mouse passive avoidance test. The role of the type 1, 2, and 3 RyR isoforms in memory processes was then evaluated by inhibiting the expression of the three RyR proteins in the mouse brain. A selective knockdown of the RyR isoforms was obtained by the i.c.v. administration of antisense oligonucleotides (aODNs) complementary to the sequence of RyR1, RyR2 and RyR3 proteins, as demonstrated by immunoblotting experiments. RyR1 (5-9 nmol per mouse i.c.v.) knockdown mice did not show any memory dysfunction. Conversely, RyR2 (1-7 nmol per mouse i.c.v.) and RyR3 (1-7 nmol per mouse i.c.v.) knockdown animals showed an impairment of memory processes. This detrimental effect was temporary and reversible, disappearing 7 d after the end of the aODN treatment. At the highest effective doses, none of the compounds used impaired motor coordination, as revealed by the rota rod test, nor modified spontaneous mobility and inspection activity, as revealed by the hole-board test. In conclusion, the lack of any involvement of cerebral RyR1 was demonstrated. These findings also showed the involvement of type 2 and type 3 RyR in the modulation of memory functions identifying these cerebral RyR isoforms as critical targets underlying memory processes.

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Section: Discussionmentioning

confidence: 99%

Different involvement of type 1, 2, and 3 ryanodine receptors in memory processes

Galeotti¹,

Quattrone²,

Vivoli³

et al. 2008

Learn. Mem.

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“…The difference observed between skeletal and cardiac muscles may due to the known presence of different ryanodine recepters in the two muscles, skeletal muscle possessing RYR-1 and RYR-3 receptors, whereas cardiac muscle possesses the RYR-2 receptor. All three types of RYR receptors may contribute to the Ca mechanism in these cells, although it was reliably reported that Cl --dependent activation of Ca 2+ release occurs through the RYR-1 receptor in skeletal muscle (27). In the case of smooth muscle cells, it has been reported that RYR-2 and RYR-3 receptor genes are both present.…”

Section: +mentioning

confidence: 98%

“…In the case of smooth muscle cells, it has been reported that RYR-2 and RYR-3 receptor genes are both present. If we assume that the RYR-2 receptor does not mediate Cl --dependent Ca 2+ release in smooth muscle cells, as it is reported to do in cardiac RYR-2 (27), then the RYR-3 receptor may mediate Ca 2+ release from the SR in smooth muscle cells. As replacement of Cl -with methanesulfonate reduced the Ca 2+ -induced Ca 2+ release in the skeletal muscle of RYR-1 knock-out mice (27), both RYR-1 and RYR-3 receptors seem to be regulated by the intracellular Cl -concentration in skeletal muscle.…”

Section: +mentioning

confidence: 99%

Chloride Channels and Their Functional Roles in Smooth Muscle Tone in the Vasculature

Kitamura

Yamazaki

2001

Japanese Journal of Pharmacology

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ABSTRACT-Although evidence of important contributions by Cl-channels to agonist-induced currents have been reported in vascular smooth muscle cells, the functional roles played by Cl -channels in the smooth muscle contraction and in setting the membrane potential remain essentially obscure. All of the admittedly few papers published have focused on the physiological roles of Cl -channels in the contraction and membrane depolarization elicited by agonists. At present, it seems likely that in vascular cells: a) Cl -conductance contributes to membrane depolarization, with the subsequent contraction being due to Ca 2+ release from the intracellular store sites, and b) Cl -movements through the membrane of the Ca 2+ store sites also regulate Ca 2+ release and Ca 2+ uptake from / into the store sites. As a Ca 2+-dependent Cl -current is most easily demonstrated under quasi-physiological conditions (by the perforated patch-clamp method), the contribution made by Cl -channels to smooth muscle function may be more important than previously thought. The development of the new, selective Cl --channel blockers as well as the identification and gene engineering of the channel molecules are essential if we are to advance our knowledge of the physiology and pharmacology of the Cl -channels residing in vascular smooth muscle cells.

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“…These experimental conditions are expected to promote the release of all the SR Ca 2+ that is releasable by caffeine [18]. Furthermore, a solution containing 10 µM free Ca 2+ releases Ca 2+ from the SR via the CICR process in mammalian skinned muscle fibers [11,15,17,19]. Here, we found that Ca 2+ /caffeine -induced Ca 2+ release in muscle fibers from mutant mice were significantly (P < 0.001) different than that displayed by muscle fibers from controls.…”

Section: Ca 2+ /Caffeine -Induced Ca 2+ Release Is Modified In Mg29 Kmentioning

confidence: 59%

“…Others and we have previously demonstrated that under experimental conditions similar to those used here, CICR is present and functional in rabbit [15], mouse [16] and rat [11] skinned muscle fibers. Endo and Takeshima [17] have also demonstrated that CICR is present and functional in skinned skeletal myocytes from mice. These authors concluded that CICR was mediated via RyR-1 and RyR-3 in mammalian skeletal muscles, because in permeabilized myocytes lacking both the RyRs, CICR mechanism was completely lost, and caffeine failed to induce Ca 2+ release [15].…”

Section: Ca 2+ /Caffeine -Induced Ca 2+ Release Is Modified In Mg29 Kmentioning

confidence: 94%

Defective maintenance of intracellular Ca2+ homeostasis is linked to increased muscle fatigability in the MG29 null mice

et al. 2004

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Mitsugumin 29 (MG29) is a transmembrane protein that is normally found in the triad junction of skeletal muscle. Our previous studies have shown that targeted deletion of mg29 from the skeletal muscle resulted in abnormality of the triad junction structure, and also increased susceptibility to muscle fatigue. To elucidate the basis of these effects, we investigated the properties of Ca 2+ -uptake and -release in toxin-skinned Extensor Digitorium Longus (EDL) muscle fibers from control and mg29 knockout mice. Compared with the control muscle, submaximal Ca 2+ -uptake into the sarcoplasmic reticulum (SR) was slower and the storage of Ca 2+ inside the SR was less in the mutant muscle, due to increased leakage process of Ca 2+ movement across the SR. The leakage pathway is associated with the increased sensitivity of Ca 2+ /caffeine -induced Ca 2+ release to myoplasmic Ca 2+ . Therefore, the increased fatigability of mutant EDL muscles can result from a combination of a slowing of Ca 2+ uptake, modification of Ca 2+ -induced Ca 2+ release (CICR), and a reduction in total SR Ca 2+ content.

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Functional and Morphological Features of Skeletal Muscle from Mutant Mice Lacking Both Type 1 and Type 3 Ryanodine Receptors

Cited by 61 publications

References 21 publications

Different involvement of type 1, 2, and 3 ryanodine receptors in memory processes

Different involvement of type 1, 2, and 3 ryanodine receptors in memory processes

Chloride Channels and Their Functional Roles in Smooth Muscle Tone in the Vasculature

Defective maintenance of intracellular Ca2+ homeostasis is linked to increased muscle fatigability in the MG29 null mice

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