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Monitoring the Effect of Osmotic Stress on Secretory Vesicles and Exocytosis
Published on: February 19, 2018
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Cold stimulation evokes exocytotic vesicle release from PC12 cells.
Biomedical Research (Tokyo, Japan)
|December 23, 2016
Summary
Low temperatures may trigger peripheral sympathetic neurons to release transmitters, potentially explaining Raynaud
Area of Science:
- Neuroscience
- Physiology
- Cell Biology
Background:
- Raynaud's phenomenon involves peripheral blood circulation failure due to cold.
- The precise mechanism underlying this cold-induced circulatory response remains unclear.
- Peripheral sympathetic neurons are implicated in regulating blood flow.
Purpose of the Study:
- To investigate if cold sensation directly triggers transmitter release from peripheral sympathetic neurons.
- To explore the cellular mechanisms involved in cold sensing by sympathetic neurons.
- To identify potential cold-responsive pathways in the regulation of peripheral circulation.
Main Methods:
- Utilized PC12 cells as a model for sympathetic neurons.
- Exposed PC12 cells to reduced temperature (25°C) and high potassium stimulation.
- Employed electron microscopy to observe cellular changes, specifically exocytotic vesicle figures.
- Compared results with control conditions (37°C).
Main Results:
- A significant increase in omega-shaped exocytotic vesicle figures was observed in PC12 cells at 25°C compared to 37°C.
- This cold-induced exocytosis was less pronounced than that induced by high potassium stimulation.
- PC12 cells and sympathetic neurons lack known cold-sensing channels (TRPA1, TRPM8).
Conclusions:
- Peripheral sympathetic neurons may possess an unidentified cold-monitoring system.
- This system likely responds to low temperatures by initiating transmitter release via exocytosis.
- This mechanism could directly influence local blood circulation, offering insight into Raynaud's phenomenon.

