Journal article
Secretion from rat neurohypophysial nerve terminals (neurosecretosomes) rapidly inactivates despite continued elevation of intracellular Ca 2
Brain research, v 574(1), pp 33-41
1992
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Abstract
Cytoplasmic calcium concentration was measured in neurosecretory nerve terminals (neurosecretosomes) isolated from rat neurohypophyses by fura-2 fluorescence measurements and digital video microscopy. Hormone release and cytoplasmic calcium concentration were measured during depolarizations induced by elevated extracellular potassium concentration. During prolonged depolarizations with 55 mM [K
+]
0, the cytoplasmic calcium concentration remained elevated as long as depolarization persisted, while secretion inactivated after the initial sharp rise. The amplitude and duration of the increase in [Ca
2+]
i was dependent on the degree of depolarization such that upon low levels of depolarizations (12.5 mM or 25 mM [K
+]
0), the calcium responses were smaller and relatively transient, and with higher levels of depolarization (55 mM [K
+]
0) the responses were sustained and were higher in amplitude. Responses to low levels of depolarization were less sensitive to the dihydropyridine calcium channel blocker, nimodipine, while the increase in [Ca
2+]
i induced by 55 mM [K
+]
0 became transient, and was significantly smaller. These observations suggest that these peptidergic nerve terminals possess at least two different types of voltage-gated calcium channels. Removal of extracellular sodium resulted in a significant increase in [Ca
2+]
i and secretion in the absence of depolarizing stimulus, suggesting that sodium-calcium exchange mechanism is operative in these nerve terminals. Although the [Ca
2+]
i increase was of similar magnitude to the depolarization-induced changes, the resultant secretion was 10-fold lower, but the rate of inactivation of secretion, however, was comparable.
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Details
- Title
- Secretion from rat neurohypophysial nerve terminals (neurosecretosomes) rapidly inactivates despite continued elevation of intracellular Ca 2
- Creators
- Alessandro Fatatis - National Institute of Child Health and Human DevelopmentLynne HoltzclawKemal PayzaJames T. Russell - National Institutes of Health
- Publication Details
- Brain research, v 574(1), pp 33-41
- Publisher
- Elsevier
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- College of Medicine; Pharmacology and Physiology; Drexel University
- Web of Science ID
- WOS:A1992HK08900005
- Scopus ID
- 2-s2.0-0026612279
- Other Identifier
- 991020100204804721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Neurosciences