Type 1 Inositol (1,4,5)-Trisphosphate Receptor Activates Ryanodine Receptor 1 to Mediate Calcium Spark Signaling in Adult Mammalian Skeletal Muscle

Tjondrokoesoemo, Andoria; Li, Na; Lin, Pei‐Hui; Pan, Zui; Ferrante, Christopher; Shirokova, Natalia; Brotto, Marco; Weisleder, Noah; Ma, Jianjie

doi:10.1074/jbc.m112.425975

Cited by 29 publications

(26 citation statements)

References 38 publications

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“…It is also worth noting that blocking RyR channels with DANT also partially inhibited the rescue of DA neurons by OXB, suggesting that ER calcium released via IP 3 R might also serve to activate RyR through a calcium-induced calcium release mechanism. Consistent with this possibility, a cross-talk between IP 3 R and RyR has already been described in skeletal muscle cells (Tjondrokoesoemo et al, 2013). Present data are also globally consistent with previous studies showing that ER calcium pools may be crucial for the control of DA cell survival in a state of chronic neurodegeneration (Cali et al, 2012;Michel et al, 2013).…”

Section: Survival Promotion Of Dopamine Neurons By Orexinsupporting

confidence: 81%

The Sleep-Modulating Peptide Orexin-B Protects Midbrain Dopamine Neurons from Degeneration, Alone or in Cooperation with Nicotine

et al. 2014

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To determine whether orexinergic hypothalamic peptides can influence the survival of brainstem dopamine (DA) neurons, we used a model system of rat midbrain cultures in which DA neurons degenerate spontaneously and progressively as they mature. We established that orexin (OX)-B provides partial but significant protection to spontaneously dying DA neurons, whereas the homologous peptide OXA has only marginal effects. Importantly, DA neurons rescued by OXB accumulated DA efficiently by active transport, suggesting that they were functional. G-proteincoupled OX1 and OX2 receptors were both present on DA neurons, but the protective effect of OXB was attributable solely to OX2 receptors; a selective inhibitor of this receptor subtype,amino]-N-(3-pyridinylmethyl)-acetamide (EMPA), suppressed this effect, whereas a selective agonist, [Ala 11 , ]OXB, reproduced it. Survival promotion by OXB required intracellular calcium mobilization via inositol-1,4,5-triphosphate and ryanodine receptors. Nicotine, a well known neuroprotective molecule for DA neurons, improved OXB-mediated rescue through the activation of a-bungarotoxin-sensitive (presumably a7) nicotinic receptors, although nicotine had no effect on its own. Altogether, our data suggest that the loss of hypothalamic orexinergic neurons that occurs in Parkinson's disease might confer an increased vulnerability to midbrain DA neurons in this disorder.

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Section: Survival Promotion Of Dopamine Neurons By Orexinsupporting

confidence: 81%

The Sleep-Modulating Peptide Orexin-B Protects Midbrain Dopamine Neurons from Degeneration, Alone or in Cooperation with Nicotine

et al. 2014

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“…In addition, recent findings show that IP 3 signaling is less prominent in adult skeletal muscle fibers compared to immature myotubes (38). However, osmotic stress transiently triggers prominent peripheral Ca 2þ sparks that occur as a result of cross talk between type I IP 3 receptors (IP 3 Rs) and type I RyRs (39). Given the peripheral localization of osmotic shock-induced Ca 2þ sparks, it is plausible that the IP 3 Rs are actually nuclear receptors (40).…”

Section: Introductionmentioning

confidence: 97%

Monovalent Cationic Channel Activity in the Inner Membrane of Nuclei from Skeletal Muscle Fibers

Yarotskyy

Dirksen

2014

Biophysical Journal

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Nuclear ion channels remain among the least studied and biophysically characterized channels. Although considerable progress has been made in characterizing calcium release channels in the nuclear membrane, very little is known regarding the properties of nuclear monovalent cationic channels. Here, we describe a method to isolate nuclei from adult skeletal muscle fibers that are suitable for electrophysiological experiments. Using this approach, we show for the first time, to our knowledge, that a nuclear monovalent cationic channel (NMCC) is prominently expressed in the inner membrane of nuclei isolated from flexor digitorum brevis skeletal muscle fibers of adult mice. In isotonic 140 mM KCl, the skeletal muscle NMCC exhibits a unitary conductance of ?160 pS and high, voltage-independent open probability. Based on single-channel reversal potential measurements, NMCCs are slightly more permeable to potassium ions over sodium (PK/PNa = 2.68 ± 0.21) and cesium (PK/PCs = 1.39 ± 0.03) ions. In addition, NMCCs do not permeate divalent cations, are inhibited by calcium ions, and demonstrate weak rectification in asymmetric Ca(2+)-containing solutions. Together, these studies characterize a voltage-independent NMCC in skeletal muscle, the properties of which are ideally suited to serve as a countercurrent mechanism during calcium release from the nuclear envelope.

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“…entry (Launikonis et al 2003) and a role in voltage-activated and voltage-independent cytosolic Ca 2? signals (Casas et al 2010;Tjondrokoesoemo et al 2013 respectively).…”

Section: Introductionmentioning

confidence: 98%

“…sparks near the periphery of the muscle fibers. Tjondrokoesoemo et al (2013) reported that osmoticstress induced Ca 2? sparks were suppressed by the inhibition of either PLC or Ins(1,4,5)P 3 receptors and were facilitated following photolysis of caged Ins(1,4,5)P 3 .…”

Section: Introductionmentioning

confidence: 99%

Phosphoinositides in Ca2+ signaling and excitation–contraction coupling in skeletal muscle: an old player and newcomers

Csernoch

Jacquemond

2015

J Muscle Res Cell Motil

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Since the postulate, 30 years ago, that phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P 2) as the precursor of inositol 1,4,5-trisphosphate (Ins(1,4,5)P 3) would be critical for skeletal muscle excitation-contraction (EC) coupling, the issue of whether phosphoinositides (PtdInsPs) may have something to do with Ca(2+) signaling in muscle raised limited interest, if any. In recent years however, the PtdInsP world has expanded considerably with new functions for PtdIns(4,5)P 2 but also with functions for the other members of the PtdInsP family. In this context, the discovery that genetic deficiency in a PtdInsP phosphatase has dramatic consequences on Ca(2+) homeostasis in skeletal muscle came unanticipated and opened up new perspectives in regards to how PtdInsPs modulate muscle Ca(2+) signaling under normal and disease conditions. This review intends to make an update of the established, the questioned, and the unknown regarding the role of PtdInsPs in skeletal muscle Ca(2+) homeostasis and EC coupling, with very specific emphasis given to Ca(2+) signals in differentiated skeletal muscle fibers.

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Type 1 Inositol (1,4,5)-Trisphosphate Receptor Activates Ryanodine Receptor 1 to Mediate Calcium Spark Signaling in Adult Mammalian Skeletal Muscle

Cited by 29 publications

References 38 publications

The Sleep-Modulating Peptide Orexin-B Protects Midbrain Dopamine Neurons from Degeneration, Alone or in Cooperation with Nicotine

The Sleep-Modulating Peptide Orexin-B Protects Midbrain Dopamine Neurons from Degeneration, Alone or in Cooperation with Nicotine

Monovalent Cationic Channel Activity in the Inner Membrane of Nuclei from Skeletal Muscle Fibers

Phosphoinositides in Ca2+ signaling and excitation–contraction coupling in skeletal muscle: an old player and newcomers

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