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Quantifying Spontaneous Ca2+ Fluxes and their Downstream Effects in Primary Mouse Midbrain Neurons
Published on: September 9, 2020
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Looping circuit: a novel mechanism for prolonged spontaneous [Ca2+]i increases in developing embryonic mouse
Hirofumi Watari1, Amanda J Tose, Martha M Bosma
1Department of Biology, Box 351800, University of Washington, Seattle, WA 98195, USA. martibee@uw.edu.
The Journal of Physiology
|December 25, 2013
Summary
In mouse brainstem development, unique calcium signaling events called "bash bursts" occur due to a propagating circuit. This transient activity influences neuronal development before disappearing.
Area of Science:
- Neuroscience
- Developmental Biology
- Calcium Signaling
Background:
- Cells typically maintain low intracellular calcium ([Ca(2+)]i).
- Transient calcium influx is usually cleared rapidly.
- Unusual, prolonged calcium events were observed in embryonic mouse brainstem.
Purpose of the Study:
- Investigate the mechanism behind 'bash bursts', a prolonged calcium signaling event.
- Understand the circuit dynamics and regulation of these bursts.
- Determine the developmental impact of this transient calcium activity.
Main Methods:
- Calcium imaging in embryonic mouse brainstem.
- Electrophysiology to record neuronal activity.
- Analysis of spontaneous calcium event propagation and duration.
Main Results:
- Bash bursts originate from a midline hindbrain event propagating in a circular circuit (3-5s laps).
- High membrane excitability and persistent inward 'window current' support these bursts.
- Bash bursts cease by embryonic day 13.5 due to circuit alterations.
Conclusions:
- A specific looping circuit in the embryonic brainstem generates prolonged intracellular calcium elevations.
- This transient, high-calcium state may regulate the development of serotonergic and dopaminergic neurons.
- The developmental window of bash bursts is critical for neuronal maturation.
