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Ca2+ Release from Subplasmalemmal Stores as a Primary Event during Exocytosis in Paramecium Cells

Christian Erxleben and Helmut Plattner
The Journal of Cell Biology
Vol. 127, No. 4 (Nov., 1994), pp. 935-945
Stable URL: http://www.jstor.org/stable/1616620
Page Count: 11
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Ca2+ Release from Subplasmalemmal Stores as a Primary Event during Exocytosis in Paramecium Cells
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Abstract

A correlated electrophysiological and light microscopic evaluation of trichocyst exocytosis was carried 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 Na in and posterior Kout currents (both known to be Ca2+-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 Ca2+ appears to be different. Current responses to AED were blocked by W7 or trifluoperazine, while exocytosis remained unaffected. Reducing [ Ca2+] o to ≤ 0.16 μM (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 Ca2+ from the subplasmalemmal pools which not only activates exocytosis (abolished by iontophoretic EGTA injection) but secondarily also spatially segregated plasmalemmal Ca2+-dependent ion channels (indicative of subplasmalemmal [ Ca2+] i increase, but irrelevant for Ca2+ mobilization). The 45 Ca2+ 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 Ca2+ mobilization from stores by mechanical coupling to the cell membrane (without previous Ca2+-influx from outside) closely resembles the model currently discussed for skeletal muscle triads.

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