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Functional coupling of secretion and capacitative calcium entry in PC12 cells
1Division of Pharmacology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya, Tokyo 158, Japan.
Biochemical and Biophysical Research Communications
|July 25, 1998
Summary
Caffeine triggers calcium release and dopamine secretion in PC12 cells by activating store-dependent calcium entry. Inhibiting calcium pumps with CPA or thapsigargin blocks these caffeine-evoked responses.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- PC12 cells are an excitable cell line commonly used to study neuronal function.
- Intracellular calcium concentration ([Ca2+]i) plays a critical role in cellular signaling and secretion.
- Caffeine is a known stimulant that can affect intracellular calcium levels.
Purpose of the Study:
- To investigate the effects of caffeine on intracellular calcium concentration ([Ca2+]i) and dopamine release in PC12 cells.
- To elucidate the role of store-dependent calcium entry in caffeine-induced secretory responses.
Main Methods:
- PC12 cells were stimulated with caffeine.
- Intracellular calcium concentration ([Ca2+]i) was measured.
- Dopamine release was assessed.
- Cells were treated with calcium pump inhibitors: cyclopiazonic acid (CPA) and thapsigargin.
Main Results:
- Caffeine induced a transient release of intracellular calcium followed by sustained calcium entry via a non-voltage-dependent pathway.
- Inhibitors of the endoplasmic reticulum Ca2+ATPase pump (CPA, thapsigargin) caused a sustained rise in [Ca2+]i and abolished subsequent caffeine responses.
- Caffeine-evoked dopamine release required extracellular calcium and was mimicked by CPA treatment.
Conclusions:
- Store-dependent calcium entry is essential for caffeine-induced dopamine secretion in PC12 cells.
- Caffeine's effects on [Ca2+]i and dopamine release are linked to the modulation of intracellular calcium stores and subsequent calcium influx.