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Endothelin Opens Potassium Channels in Glial Cells
Surachai Supattapone1, Christopher C. Ashley
1University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, UK.
The European Journal of Neuroscience
|January 1, 1991
Summary
Endothelin-1 and endothelin-3 activate a calcium-dependent potassium channel in glial cells. This finding suggests endothelins may mediate astroglial responses to brain injury.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Endothelin-1 (ET-1), synthesized by astrocytes, and endothelin-3 (ET-3), produced by neurons, are known to stimulate astrocyte proliferation.
- Previous studies indicated endothelins' role in astrocyte growth.
Purpose of the Study:
- To investigate the effect of ET-1 and ET-3 on ion channel activity in glial cells.
- To determine if endothelins can modulate ion flux relevant to the brain microenvironment.
Main Methods:
- Utilized 86Rubidium (86Rb+) influx assays to measure ion transport.
- Employed single-channel patch-clamp recording to analyze ion channel function.
- Investigated charybdotoxin-sensitive, calcium-activated potassium channels.
Main Results:
- Both ET-1 and ET-3 were demonstrated to open a specific type of potassium channel in glial cells.
- The identified channel is calcium-activated and sensitive to charybdotoxin, with a conductance of 15-40 pS.
- This channel opening is a novel effect of endothelins on glial cells.
Conclusions:
- Endothelin-1 and endothelin-3 can activate a calcium-dependent potassium channel in glial cells.
- The modulation of this potassium channel by endothelins may play a role in regulating extracellular potassium ([K+]) in the brain.
- Endothelins might serve as general mediators of astroglial responses to neuronal injury.
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