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Cellular calcium handling in brain slices from calbindin D28k-deficient mice
L Pasti1, G Carmignoto, T Pozzan
1Department of Experimental Biomedical Sciences, University of Padova, Italy.
Neuroreport
|August 10, 1999
Summary
Calbindin D28k deficiency in neurons causes prolonged calcium signal elevation upon depolarization. This effect is specific to brain regions with reduced calbindin D28k levels, indicating its crucial role in neuronal calcium regulation.
Area of Science:
- Neuroscience
- Cellular Biology
- Molecular Biology
Background:
- Calbindin D28k is a neuronal calcium-binding protein.
- Its precise role in regulating intracellular calcium dynamics during neuronal activity is not fully understood.
Purpose of the Study:
- To investigate the role of calbindin D28k in cellular calcium handling in the brain.
- To examine how a deficiency in calbindin D28k affects neuronal calcium responses to depolarization.
Main Methods:
- Utilized transgenic antisense mice with a regional deficiency in calbindin D28k.
- Compared brain slices from these mice with non-transgenic wild-type littermate controls.
- Stimulated brain slices with NMDA or potassium to induce depolarization and measured neuronal calcium signals.
Main Results:
- Depolarization led to a prolonged elevation of neuronal calcium signals in calbindin D28k-deficient transgenic mice.
- This effect was regionally selective, observed only in areas with significant calbindin D28k depletion.
- Glial cells and neurons in other brain regions showed normal calcium handling.
Conclusions:
- Calbindin D28k plays a critical role in buffering neuronal calcium levels during depolarization.
- Regional deficiency of calbindin D28k impairs cellular calcium handling, leading to prolonged calcium signal elevations.
- These findings highlight the importance of calbindin D28k in maintaining neuronal calcium homeostasis.