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Published on: October 13, 2014
Caffeine-sensitive Ca2+ stores in carp retinal bipolar cells
1Unit of Cell Signal Transduction, Shanghai Institute of Physiology, Chinese Academy of Sciences.
Neuroreport
|March 15, 2000
Summary
High potassium and caffeine trigger calcium signals in carp retinal ON-type bipolar cells. Calcium influx via L-type channels is crucial for potassium-induced signals, while caffeine releases calcium from somatic stores.
Area of Science:
- Neuroscience
- Cell Biology
- Ophthalmology
Background:
- Retinal bipolar cells are key interneurons in visual processing.
- Understanding calcium signaling dynamics is crucial for photoreceptor function.
Purpose of the Study:
- To investigate the sources and mechanisms of intracellular calcium ([Ca2+]i) increases in carp retinal ON-type bipolar cells.
- To differentiate the roles of voltage-gated calcium channels and intracellular calcium stores in response to stimuli.
Main Methods:
- Confocal laser-scanning microscopy was used to monitor [Ca2+]i.
- Cells were stimulated with high potassium (35 mM) and caffeine (100 microM).
- Pharmacological agents like nifedipine and ryanodine were employed to block specific channels and receptors.
Main Results:
- High K+ induced [Ca2+]i rise in both soma and terminal, dependent on external Ca2+ and L-type Ca2+ channels.
- Caffeine-induced [Ca2+]i elevation was restricted to the soma and blocked by ryanodine, indicating ryanodine-sensitive stores.
- Ryanodine treatment reduced high K+-evoked Ca2+ transients in the soma, suggesting cross-talk between influx and release.
Conclusions:
- Depolarization-evoked Ca2+ influx can trigger Ca2+ release from somatic caffeine-sensitive stores.
- This release mechanism amplifies the Ca2+ signal in the soma of retinal bipolar cells.
- Distinct mechanisms govern calcium signaling in the soma versus the terminal of these cells.
