Abstract
In NG108-15 cells, bradykinin (BK) and thapsigargin (TG) caused transient increases in a cytosolic free Ca2+ concentration ([Ca2+]i), after which [Ca2+]i elevated by TG only declined to a higher, sustained level than an unstimulated level. In PC12 cells, carbachol (CCh) evoked a transient increase in [Ca2+]i followed by a sustained rise of [Ca2+]i, whereas [Ca2+]i elevated by TG almost maintained its higher level. In the absence of extracellular Ca2+, the sustained elevation of [Ca2+]i induced by each drug we used was abolished. In addition, the rise in [Ca2+]i stimulated by TG was less affected after CCh or BK, whereas CCh or BK caused no increase in [Ca2+]i after TG. TG neither increased cellular inositol phosphates nor modified the inositol phosphates format on stimulated by CCh or BK. We conclude that TG may release Ca2+ from both IP3-sensitive and -insensitive intracellular pools and that some kinds of signalling to link the intracellular Ca2+ pools and Ca2+ entry seem to exist in neuronal cells.
| Original language | English |
|---|---|
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 180 |
| Issue number | 3 |
| Pages (from-to) | 1518-26 |
| Number of pages | 9 |
| ISSN | 0006-291X |
| Publication status | Published - 1991 |
| Externally published | Yes |
Keywords
- Animals
- Biological Transport
- Bradykinin
- Calcium
- Calcium Channel Blockers
- Cell Line
- Cell Membrane
- Fluorescent Dyes
- Fura-2
- Glioma
- Inositol 1,4,5-Trisphosphate
- Inositol Phosphates
- Kinetics
- Neuroblastoma
- Nimodipine
- PC12 Cells
- Peptides, Cyclic
- Terpenes
- Thapsigargin
- omega-Conotoxins