Intracellular calcium and vasopressin release of rat isolated neurohypophysial nerve endings.

Stuenkel, Edward L.; Nordmann, J

doi:10.1113/jphysiol.1993.sp019775

Cited by 41 publications

(33 citation statements)

References 63 publications

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“…Studies in cortical synaptosomes suggest a similar pattern of coupling of presynaptic opioid receptors to Ca 2ϩ channels, in that here both N-and L-type channels contribute to depolarization-evoked Ca 2ϩ entry, whereas the inhibitory effects of -opioid agonists on [C a 2ϩ ] i and exocytosis are blocked by GV IA but not by dihydropyridines (Adamson et al, 1989;X iang et al, 1990). However, L -type channels have been shown in chromaffin cells to be more efficiently coupled to exocytosis than N-and P-type channels (Artalejo et al, 1994) and similarly play an important role in neurohormone release in rat neurosecretory endings (Stuenkel and Nordmann, 1993). It is not surprising, therefore, that L channels are the target for G-protein modulation in melanotrophs from rat pituitary gland (Ciranna et al, 1996) and that they are most sensitive to modulation by -opioids in isolated neurohypophysial nerve terminals as reported here.…”

Section: Discussionmentioning

confidence: 96%

κ-Opioid Receptor Activation Modulates Ca²⁺Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

et al. 1997

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Whole-cell patch-clamp recordings were performed together with time-resolved measurements of membrane capacitance (C m ) in nerve terminals acutely dissociated from neurohypophysis of adult rats to investigate modulation of Ca 2ϩ currents and secretion by activation of opioid receptors. Bath superfusion of the -opioid agonists U69,593 (0.3-1 M), dynorphin A (1 M), or U50,488H (1-3 M) reversibly suppressed the peak amplitude of Ca 2ϩ currents 32.7 Ϯ 2.7% (in 41 of 56 terminals), 37.4 Ϯ 5.3% (in 5 of 8 terminals), and 33.5 Ϯ 8.1% (in 5 of 10 terminals), respectively. In contrast, tests in 11 terminals revealed no effect of the -opioid agonist [D-Pen 2,5 ]-enkephalin (1-3 M; n ϭ 7) or of the ␦-agonist Tyr-D-Ala-Gly-N-Me-PheGly-ol (1 M; n ϭ 4) on Ca 2ϩ currents. Three components of high-threshold current were distinguished on the basis of their sensitivity to blockade by -conotoxin GVIA, nicardipine, and -conotoxin MVIIC: N-, L-, and P/Q-type current, respectively.Administration of U69,593 inhibited N-type current in these nerve terminals on average 32%, whereas L-type current was reduced 64%, and P/Q-type current was inhibited 28%. Monitoring of changes in C m in response to brief depolarizing steps revealed that the -opioid-induced reductions in N-, L-, or P/Q-type currents were accompanied by attenuations in two kinetically distinct components of Ca 2ϩ -dependent exocytotic release. These data provide strong evidence of a functional linkage between blockade of Ca 2ϩ influx through voltagedependent Ca 2ϩ channels and inhibitory modulation of release by presynaptic opioid receptors in mammalian central nerve endings.

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Section: Discussionmentioning

confidence: 96%

κ-Opioid Receptor Activation Modulates Ca²⁺Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

et al. 1997

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“…In the present work, we add the observation that after 20 min of continuous potassium challenge, the increase in Ca v is even larger than at 6 min. Under such conditions of potassium depolarization, it has been shown by imaging of individual neurohypophysial nerve terminals that free cytosolic Ca concentration ([Ca 2ϩ ] i ), after the initial rise, stabilizes at a plateau around 400-500 nM (24). However, even with continuous depolarization and high [Ca 2ϩ ] i , neurohypophysial terminals will only briefly release their secretory products (4,5).…”

Section: Intravesicularmentioning

confidence: 99%

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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“…Frequencydependent action-potential broadening is thought to be one of the mechanisms involved in this pattern-dependent regulation of secretion (Gainer et al, 1986;Bourque, 1990;Jackson et al, 1991). Buildup of residual calcium levels during bursts of action potentials is considered another contributing factor (Jackson et al, 1991;Stuenkel and Nordmann, 1993;Stuenkel, 1994). In addition, P/Qtype Ca 2ϩ -channels are expressed in AVP terminals, but not OXT terminals, and are believed to play a direct role in AVP secretion in the rat (Wang et al, 1997).…”

Section: Abstract: Calcium Dynamics; Excitation-secretion Coupling; mentioning

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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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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Intracellular calcium and vasopressin release of rat isolated neurohypophysial nerve endings.

Abstract: 9. These results show that the amount and duration of depolarization-induced vasopressin secretion from isolated nerve endings may be regulated not only by the absolute increase but also by periodic changes in [Ca2+]i.

Cited by 41 publications

References 63 publications

κ-Opioid Receptor Activation Modulates Ca²⁺Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

κ-Opioid Receptor Activation Modulates Ca²⁺Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

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

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

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Intracellular calcium and vasopressin release of rat isolated neurohypophysial nerve endings.

Abstract: 9. These results show that the amount and duration of depolarization-induced vasopressin secretion from isolated nerve endings may be regulated not only by the absolute increase but also by periodic changes in [Ca2+]i.

Cited by 41 publications

References 63 publications

κ-Opioid Receptor Activation Modulates Ca2+Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

κ-Opioid Receptor Activation Modulates Ca2+Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

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

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

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κ-Opioid Receptor Activation Modulates Ca²⁺Currents and Secretion in Isolated Neuroendocrine Nerve Terminals

κ-Opioid Receptor Activation Modulates Ca²⁺Currents and Secretion in Isolated Neuroendocrine Nerve Terminals