Ryanodine modifies conductance and gating behavior of single Ca2+ release channel

Rousseau, Éric; Smith, Jeffrey S.; Meissner, Gerhard

doi:10.1152/ajpcell.1987.253.3.c364

Cited by 551 publications

(352 citation statements)

References 22 publications

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“…In contrast, ryanodine produces a slower but sustained increase in [Cali that persists long after drug removal, again in agreement with studies on the native tissue. This behavior of ryanodine is consistent with the observation that it induces a persistent, but partial activation of the ryanodine receptor channel reconstituted in planar lipid bilayers [20,21].…”

Section: Discussionsupporting

confidence: 90%

Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA

et al. 1989

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Combined patch-clamp and fura-measurements were performed to study the calcium release properties of Chinese hamster ovary (CHO) cells transfected with the rabbit skeletal muscle ryanodine receptor cDNA carried by an expression vector. Both caffeine (l-50 mM) and ryanodine (100 PM) induced release of calcium from intracellular stores of transformed CHO cells but not from control (non-transfected) CHO cells. The calcium responses to caffeine and ryanodine closely resembled those commonly observed in skeletal muscle. Repetitive applications of caffeine produced characteristic all-or-none rises in intracellular calcium. Inositol 1,4,5trisphosphate (IPJ neither activated the ryanodine receptor channel nor interfered with the caffeine-elicited calcium release. These results indicate that functional calcium release channels are formed by expression of the ryanodine receptor cDNA.cDNA expression; Ryanodine receptor; Calcium release channel; Caffeine; Fura-2; (Chinese hamster ovary cell)

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Section: Discussionsupporting

confidence: 90%

Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA

et al. 1989

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“…To test for the involvement of a RyR-mediated Ca 2ϩ release mechanism, cells were preincubated with an antagonizing concentration of ryanodine before NO application. The binding of ryanodine to RyRs is practically irreversible, and at doses Ͼ50 M, the associated Ca 2ϩ conductance is inhibited (Rousseau et al, 1987;Zimanyi et al, 1992). Because of its slow association kinetics (Pessah et al, 1987), a ryanodine concentration of 100 M and preincubation of 30 min was used.…”

Section: Nitric Oxide Induces Ca 2؉ Mobilization In Glial Cells Via Tmentioning

confidence: 99%

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca²⁺Waves in Glia

2000

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In this study, we highlight a role for the nitric oxide-cGMPdependent protein kinase (NO-G-kinase) signaling pathway in glial intercellular Ca 2ϩ wave initiation and propagation. Addition of the NO donor molsidomine (100-500 M) or puffing aqueous NO onto primary glial cell cultures evoked an increase in [Ca 2ϩ ] i in individual cells and also local intercellular Ca 2ϩ waves, which persisted after removal of extracellular Ca 2ϩ . High concentrations of ryanodine (100-200 M) and antagonists of the NO-G-kinase signaling pathway essentially abrogated the NO-induced increase in [Ca 2ϩ ] i , indicating that NO mobilizes Ca 2ϩ from a ryanodine receptor-linked store, via the NO-G-kinase signaling pathway. Addition of 10 M nicardipine to cells resulted in a slowing of the molsidomine-induced rise in [Ca 2ϩ ] i , and inhibition of Mn 2ϩ quench of cytosolic fura-2 fluorescence mediated by a bolus application of 2 M aqueous NO to cells, indicating that NO also induces Ca 2ϩ influx in glia. Mechanical stress of individual glial cells resulted in an increase in intracellular NO in target and neighboring cells and intercellular Ca 2ϩ waves, which were NO, cGMP, and G-kinase dependent, because incubating cells with nitric oxide synthase, guanylate cyclase, and G-kinase inhibitors, or NO scavengers, reduced ⌬[Ca 2ϩ ] i and the rate of Ca 2ϩ wave propagation in these cultures. Results from this study suggest that NO-Gkinase signaling is coupled to Ca 2ϩ mobilization and influx in glial cells and that this pathway plays a fundamental role in the generation and propagation of intercellular Ca 2ϩ waves in glia. Key words: nitric oxide; glia; calcium waves; mobilization; influx; ryanodine receptors; nitric oxide synthase; DAF-2; phospholipase C; astrocytesIt is becoming increasingly apparent that intercellular Ca 2ϩ waves might be the result of combined contributions of intracellular and extracellular Ca 2ϩ signaling pathways in glial cells. One generally accepted mode of intercellular Ca 2ϩ wave propagation involves the diffusion of Ca 2ϩ mobilizing second messengers, including inositol-1,4,5-trisphosphate (IP 3 ) and Ca 2ϩ , across gap junctions (Nedergaard, 1994;Charles, 1998). Extracellular, gap junction-independent modes of Ca 2ϩ signaling, involving the release of a diffusible messengers, also appear to operate in this particular system however, with ATP release from cells and P 2 receptor-coupled elevation of [Ca 2ϩ ] i having recently been suggested as a likely candidate (Cotrina et al., 1998;Guthrie et al., 1999). There are however other species that may participate as extracellular messengers in glial intercellular Ca 2ϩ waves. There is increasing evidence that the highly diffusible messenger nitric oxide (NO) can induce Ca 2ϩ mobilization in several cell types (Publicover et al., 1993; Willmott et al., 1995a,b,c;Clementi et al., 1996) either via the cGMP-dependent protein kinase (G-kinase)-coupled activation of ADP-ribosyl cyclase, resulting in an increased synthesis of the potent Ca 2ϩ mobilizing agent cyclic ADP-rib...

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“…The current is responsible for delayed afterdepolarizations and triggered activity (HOFFMAN and ROSEN, 1981). There is evidence that ryanodine acts on cardiac muscle apparently through a single mechanism, i.e., the inhibition of Ca2 + release from the SR (SuTKO and KENYON, 1983) by modulating the calcium release channels of cardiac SR membrane (ROUSSEAU et al, 1987) and that the drug does not affect the slow inward Ca2 + current (SUTKO and KENYON, 1983). In addition, caffeine in high concentrations (5-15 mM) prevents SR function by increasing the release of Ca2 from the SR, and eventually abolishes the oscillatory release of Ca2 + from the SR (FABIATO and FABIATO, 1975).…”

Section: Discussionmentioning

confidence: 99%

Two differential mechanisms of automaticity in diseased human atrial fibers.

et al. 1988

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The ionic mechanisms of automaticity in spontaneously active preparations (n = 38) from "diseased" human atria were investigated. The cycle length (CL) of the automatic action potential (AAP) ranged from 0.6 to 4.5 s (mean + S.D.: 2.0 + 1.0 s). The AAP from preparations obtained from non-digitalized patients (group 1, n = 29) showed various CLs, in that 16 patients had a CL longer than 2.0 s (slow-type AAP) while in tissues from the other 13 patients, the CL was 2.0 s or less (fast-type AAP). On the other hand, all preparations obtained from the digitalized patients prior to cardiac surgery (group 2, n = 9) had the fast-type AAP (CL <_ 2.0 s). The slow-type AAP was accelerated and changed to the fast one after application of ouabain (1 µM) or by perfusing with 50% [Na + ]o Tyrode solution. Ryanodine (1 tiM), a specific inhibitor of calcium release from the sarcoplasmic reticulum (SR), markedly lengthened the CL of fast-type AAP, without affecting the slow-type AAP. In contrast, caffeine (15 mM) shortened the CL of the slow-type AAP and remarkably lengthened the CL of the fast-type AAP, as is the case in ryanodine. The rate of slow-type AAP was enhanced with an increase in [Ca2+]o and depressed with a decrease in [Ca2 +]o or with application of diltiazem, a Ca2 + channel blocker. The slow-type AAP was changed to the fast-type AAP by stretching the preparation by about 20%. In vitro preparations excised from patients with dilated atria revealed a shorter CL of AAPs. We conclude that in "diseased" human atrial preparations, the ionic mechanism responsible for generation of slow-and fast-type automaticity differs. Slow automaticity (CL >2.0 s) perhaps relates to activation of the slow inward Ca2 + current, while the fast-type automaticity (CL <2.0 s) is linked to cyclic increases in [Ca2 +]~.

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Ryanodine modifies conductance and gating behavior of single Ca2+ release channel

Cited by 551 publications

References 22 publications

Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA

Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca²⁺Waves in Glia

Two differential mechanisms of automaticity in diseased human atrial fibers.

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Ryanodine modifies conductance and gating behavior of single Ca2+ release channel

Cited by 551 publications

References 22 publications

Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA

Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca2+Waves in Glia

Two differential mechanisms of automaticity in diseased human atrial fibers.

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A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca²⁺Waves in Glia