Abstract：
:Ca2+ influx into secretory cells of the intact salivary gland of the blowfly Calliphora erythrocephala elicited by the agonist 5-hydroxytryptamine (5-HT) or the Ca2+ uptake inhibitor thapsigargin was studied by using Fura-2 and digital fluorescence imaging and by recordings of the transepithelial potential. Application of saturating [5-HT] in the absence of Ca2+ (Ca2+o) from the bathing saline did not affect the initial Ca2+ transient but greatly attenuated the subsequent sustained Ca2+ elevation observed in the presence of Ca2+o demonstrating that the latter component of the [Ca2+]i response is largely dependent on Ca2+ entry across the baso-lateral plasma membrane. La3+ or Gd3+ (10 microM) mimicked the effects of the withdrawal of Ca2+o. Experimental attempts temporally to uncouple 5-HT stimulation and Ca2+ influx by withdrawal of Ca2+o during agonist application revealed a second Ca2+ entry pathway. This pathway was insensitive to 10 microM La3+ and produced transient [Ca2+]i increases whose amplitudes were a function of the [5-HT] during the preceding stimulation and that were selectively suppressed by 50 microM SK&F 96365. Both (10 microM) La(3+)-insensitive [Ca2+]i transients and (10 microM) La3+ inhabitable tonic [Ca2+]i increases could be sequentially activated in the presence of 5-HT or thapsigargin (1 microM). These results indicate that Ca2+ store depletion by 5-HT or thapsigargin activates two distinct store-operated Ca2+ entry pathways, one of which supports tonic [Ca2+]i increases. The other is transiently activated, even under conditions that prohibit store refilling and does not significantly contribute to the [Ca2+]i responses evoked by saturating 5-HT concentrations.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Zimmermann Bdoi
10.1016/s0143-4160(98)90074-4subject
Has Abstractpub_date
1998-01-01 00:00:00pages
53-63issue
1eissn
0143-4160issn
1532-1991pii
S0143-4160(98)90074-4journal_volume
23pub_type
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