Effects of compound   on the Ca2+ release by reversal of the Ca2+ pump and by the Ca2+ channel of sarcoplasmic reticulum membranes

Vale, M.G.P.

doi:10.1016/0003-9861(90)90491-g

Cited by 4 publications

(3 citation statements)

References 35 publications

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“…Effect of trifluoperazine on the Ca2" release from SR It has been reported that some CaM antagonists potentiate the Ca2+ release from the SR vesicles of skeletal muscle (Meissner, 1986;Palade, 1987;Wyskovsky et al, 1988;Vale, 1990). Therefore we first examined the effect of trifluoperazine (TFP) on the Ca2+ release in skinned fibres.…”

Section: Resultsmentioning

confidence: 99%

“…All the CaM antagonists and CaM binding peptides we tested potentiated the Ca2" release from the SR. Several CaM antagonists were reported to enhance the CICR from isolated SR vesicles (Meissner, 1986;Palade, 1987;Wyskovsky et al, 1988;Vale, 1990) and the open probability of a Ca2" release channel incorporated into a lipid bilayer was increased by the presence of a high concentration of W-7 (Smith et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

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Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca²⁺‐induced Ca²⁺ release

Ikemoto

lino

Endo

1996

British J Pharmacology

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1 Calmodulin (CaM) has a biphasic effect on Ca2 -induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR): potentiation and inhibition at low (pCa>6.0) and high (pCa 5) Ca2+ concentrations, respectively. To characterize the mode of action of CaM, we studied the effect of CaM antagonists on the CICR in skinned muscle fibres of the rabbit. Ca2+ release was measured by microfluorometry with Fura-2. 2 A CaM antagonist, trifluoperazine (TFP), potentiated the CICR in a dose-dependent manner (10-300 tM) at pCa 6, where a simple reversal of the CaM effect would be inhibition of the CICR.Furthermore, 100 yM TFP sensitized the CICR to Ca2+. A similar effect was produced by other CaM antagonists that were tested: chlorpromazine, W-7, mastoparan, and peptide fragment of CaM-binding residues of CaM-dependent protein kinase II. 3 The biphasic effect of CaM on the CICR was observed even in the presence of high concentrations of CaM antagonists or CaM-binding peptides. 4 From these results we suggest that CaM has a unique mode of action on the CICR which is quite different from the effect of CaM on known enzymes.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca²⁺‐induced Ca²⁺ release

Ikemoto

lino

Endo

1996

British J Pharmacology

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“…Interestingly, footlike connections, as in Paramecium, are widely distributed also in invertebrate muscles (26). As from alveolar sacs in Paramecium, caffeine can release Ca ~+ from the so strikingly similar SR (30,39,54,55), as can various polyamines (10,19,21,39,66). Also in mast cells or pancreatic acinar cells exogenous polyamines liberate internal Ca 2+ (18,32).…”

Section: Possible Role Of Ca Storesmentioning

confidence: 99%

Ca2+ release from subplasmalemmal stores as a primary event during exocytosis in Paramecium cells.

Erxleben

Plattner

1994

The Journal of Cell Biology

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Abstract. A correlated electrophysiological and light microscopic evaluation of trichocyst exocytosis was carded out with Paramecium cells which possess extensive cortical Ca stores with footlike links to the plasmalemma. We used not only intra-but also extracellular recordings to account for polar arrangement of ion channels (while trichocysts can be released from all over the cell surface). With three widely different secretagogues, aminoethyldextran (AED), veratridine and caffeine, similar anterior Nain and posterior Kout currents (both known to be Ca 2+-dependent) were observed. Direct de-or hyperpolarization induced by current injection failed to trigger exocytosis. For both, exocytotic membrane fusion and secretagogue-induced membrane currents, sensitivity to or availability of Ca 2÷ appears to be different. Current responses to AED were blocked by W7 or trifluoperazine, while exocytosis remained unaffected.Reducing [Ca2÷]o to <0.16/zM (i.e., resting [Ca2÷]i) suppressed electrical membrane responses triggered with AED, while we had previously documented normal exocytotic membrane fusion. From this we conclude that the primary effect of AED (as of caffeine) is the mobilization of Ca 2+ from the subplasmalemmal pools which not only activates exocytosis (abolished by iontophoretic EGTA injection) but secondarily also spatially segregated plasmalemmal Ca:+-dependent ion channels (indicative of subplasmalemmal [Ca2+]i increase, but irrelevant for Ca 2÷ mobilization). The 45Ca2÷ influx previously observed during AED triggering may serve to refill depleted stores. Apart from the insensitivity of our system to depolarization, the mode of direct Ca :÷ mobilization from stores by mechanical coupling to the cell membrane (without previous Ca 2÷-influx from outside) closely resembles the model currently discussed for skeletal muscle triads.T HERE is ample evidence that exocytosis regulation follows similar principles in all cells-from protozoan to mammalian-though with variations of the basic theme (for reviews see 6, 41). The ciliated protozoan Paramecium is a favorable model system because about 103 trichocysts are docked at the cell membrane (42). This allows their synchronous release within about 0.1 s (23) in response to different secretagogues, such as polyamines (40, 43, 45), veratridine (24), or caffeine CKlauke, N., and H. Plattner. 1993. Eur. J. Cell Biol. 60[suppl.]37:142). Paramecium cells possess extended subplasmalemmal Ca-storage compartments, the alveolar sacs (61). These underly almost all of the nonciliary (i.e., somatic) cell surface, except for sites occupied by cilia or trichocysts (1, 42).Ca 2÷ plays a pivotal role in the regulation of exocytotic membrane fusion (for a review see reference 7) also in Paramecium (42) where the source of Ca 2÷ is still under debate. Based on theoretical considerations, polyamines were proposed by Cohen and Kerboeuf (11) to activate hyperpolari-

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Compound 48/80 blocks transmission and increases the excitability of ganglion neurons

Heppner

Fiekers

1992

European Journal of Pharmacology

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Effects of compound on the Ca2+ release by reversal of the Ca2+ pump and by the Ca2+ channel of sarcoplasmic reticulum membranes

Cited by 4 publications

References 35 publications

Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca²⁺‐induced Ca²⁺ release

Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca²⁺‐induced Ca²⁺ release

Ca2+ release from subplasmalemmal stores as a primary event during exocytosis in Paramecium cells.

Compound 48/80 blocks transmission and increases the excitability of ganglion neurons

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Effects of compound on the Ca2+ release by reversal of the Ca2+ pump and by the Ca2+ channel of sarcoplasmic reticulum membranes

Cited by 4 publications

References 35 publications

Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca2+‐induced Ca2+ release

Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca2+‐induced Ca2+ release

Ca2+ release from subplasmalemmal stores as a primary event during exocytosis in Paramecium cells.

Compound 48/80 blocks transmission and increases the excitability of ganglion neurons

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Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca²⁺‐induced Ca²⁺ release

Effect of calmodulin antagonists on calmodulin‐induced biphasic modulation of Ca²⁺‐induced Ca²⁺ release