Calcium‐induced calcium increase in secretory vesicles of permeabilized rat neurohypophysial nerve terminals

Troadec, Jean‐Denis; Thirion, Sylvie; Laugier, Jean-Pierre; Nicaise, Ghislain

doi:10.1111/j.1768-322x.1998.tb01043.x

Cited by 11 publications

(10 citation statements)

References 56 publications

(35 reference statements)

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“…Mitochondrial Ca 2ϩ uptake during exocytosis has also been observed in bullfrog presynaptic peptidergic terminals (Peng, 1998). Secretory granules themselves might contribute to Ca 2ϩ uptake in nerve terminals as well (Troadec et al, 1998). These findings would suggest that the slow extrusion in our data is associated with a plasmalemmal Ca 2ϩ ATPase, whereas the fast component(s) reflects high-capacity, low-affinity uptake processes inside the terminals.…”

Section: ؉ Extrusion And/or Uptakecontrasting

confidence: 44%

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Dependence of Transient and Residual Calcium Dynamics on Action-Potential Patterning during Neuropeptide Secretion

Muschol¹,

Salzberg

2000

J. Neurosci.

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Secretion of the neuropeptide arginine vasopressin (AVP) from the neurohypophysis is optimized by short phasic bursts of action potentials with a mean intraburst frequency around 10 Hz. Several hypotheses, most prominently action-potential broadening and buildup of residual calcium, have been proposed to explain this frequency dependence of AVP release. However, how either of these mechanisms would optimize release at any given frequency remains an open question. We have addressed this issue by correlating the frequency-dependence of intraterminal calcium dynamics and AVP release during action-potential stimulation.By monitoring the intraterminal calcium changes with lowaffinity indicator dyes and millisecond time resolution, the signal could be dissected into three separate components:

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Section: ؉ Extrusion And/or Uptakecontrasting

confidence: 44%

“…Indeed, loading of Fura-2 into the subcellular compartments of the rat neurohypophysis has been reported (Troadec et al, 1998). If compartmentalization occurs with Mag-Fluo-4, it does not appear to contribute to the stimulation-induced fluorescence changes.…”

Section: Methodsmentioning

confidence: 99%

Dependence of Transient and Residual Calcium Dynamics on Action-Potential Patterning during Neuropeptide Secretion

Muschol¹,

Salzberg

2000

J. Neurosci.

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“…4B). Na ϩ ͞Ca 2ϩ exchange has been characterized by biochemical techniques on isolated bovine neurosecretory vesicles (27) and by fluorescent probe imaging on permeabilized rat neurohypophysial terminals (23). Saturation of the intravesicular Ca-binding molecules (32) can raise intravesicular Ca 2ϩ concentration to values that will trigger reverse mode Na ϩ ͞Ca 2ϩ exchange.…”

Section: Discussionmentioning

confidence: 99%

“…Sci. USA 96 (1999)terminals, high cytosolic Ca, which is a known consequence of potassium depolarization, is probably at the origin of high Ca v (9,13,23). We have shown previously that if the potassium challenge was discontinued after 6 min, Ca v returned to control levels (9).…”

Section: Intravesicularmentioning

confidence: 98%

Stimulus–secretion coupling in neurohypophysial nerve endings: A role for intravesicular sodium?

Thirion

Jd²,

Nb³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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It is generally accepted that Ca is essentially involved in regulated secretion, but the role of this cation, as well as others such as Na, is not well understood. An illustrative example occurs in neurohypophysial secretion, where an experimentally induced increase in the cytosolic concentration of Na ؉ can induce continuous neuropeptide release. In contrast, an increase in cytosolic Ca 2؉ will have only a transient stimulatory effect. The secretion-promoting targets for Ca 2؉ are not known; they may be cytosolic, as is usually assumed, but they may also be intravesicular, especially in view of evidence that Ca-rich secretory vesicles are preferentially secreted. In the present work, we have investigated the movements of these cations into and out of secretory vesicles during stimulus-secretion coupling. Isolated rat neurohypophysial nerve endings were stimulated by potassium (55 mM) depolarization, and at 6 min (peak secretion) and 20 min after the onset of stimulation, the elemental content of individual secretory vesicles was measured by quantitative x-ray microanalysis. A depolarization-induced transient increase in intravesicular Na ؉ concentration was found to coincide with the onset of secretion. Moreover, only a predicted small fraction of peripheral vesicles-presumably the docked ones-were Na ؉ -loaded. The low sulfur concentration of Na ؉ -rich vesicles most likely resulted from vesicle swelling. The results suggest that high intravesicular Na ؉ concentrations in docked vesicles, occurring by Na ؉ ͞Ca 2؉ exchange or by transient fusion pore opening, is a proximal event in exocytosis. Ca 2ϩplays an essential role in several stimulatory, and perhaps also inhibitory, steps of regulated exocytosis but, despite much recent progress, its precise targets are still largely a matter of debate (1-3). In neurohypophysial secretion particularly, it is clear that Ca 2ϩ cannot be the ultimate and sufficient trigger for neurosecretion, because the obligatory depolarizationinduced increase in cytosolic Ca 2ϩ concentration stimulates release for only a few minutes (4, 5), even when depolarization is maintained. This behavior contrasts with the known but mechanistically obscure secretagogue effect of Na ϩ (6-8), wherein an artificially induced increase in cytosolic Na ϩ concentration can induce a sustained and continuous secretion (8). In previous work on neurohypophysial nerve endings, one of our laboratories reported that the Ca content of the secretory vesicles increased upon secretory stimulation, and that Ca-rich vesicles accumulated when secretion was blocked (9), suggesting a role of intravesicular ion concentration in the secretory mechanism. This hypothesis is further supported by observation that in insulin-secreting cells, Ca 2ϩ depletion from secretory granules inhibits exocytosis (10). Because the swelling of some granule matrices is inhibited by Ca 2ϩ and promoted by Na ϩ (11, 12), we have investigated in isolated and stimulated rat neurohypophysial nerve endings possible changes in the concentra...

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“…Regarding alternative Ca 2+ transport systems in the granules, the presence of either Ca 2+ -ATPases, Na + /Ca 2+ or H + /Ca 2+ exchange systems have been proposed in different preparations [14][15][16][17][18]. Inhibition of sarcoendoplasmic reticulum Ca 2+ -ATPase with 10 M benzohydroquinone produced little effects on [Ca 2+ ] SG (data not shown), suggesting that this type of Ca 2+ -ATPase was not involved.…”

Section: Dynamic Measurements Of [Ca 2+ ] In the Secretory Vesiclesmentioning

confidence: 99%

Calcium dynamics in catecholamine-containing secretory vesicles

et al. 2005

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Calcium‐induced calcium increase in secretory vesicles of permeabilized rat neurohypophysial nerve terminals

Cited by 11 publications

References 56 publications

Dependence of Transient and Residual Calcium Dynamics on Action-Potential Patterning during Neuropeptide Secretion

Dependence of Transient and Residual Calcium Dynamics on Action-Potential Patterning during Neuropeptide Secretion

Stimulus–secretion coupling in neurohypophysial nerve endings: A role for intravesicular sodium?

Calcium dynamics in catecholamine-containing secretory vesicles

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