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Cytoplasmic calcium buffer, calbindin-D28k, is regulated by excitatory amino acids
C Batini1, M Palestini, M Thomasset
1Laboratoire de physiologie de la motricité, CNRS, Université Pierre et Marie Curie, CHU Pitié-Salpêtrière, Paris, France.
Neuroreport
|July 1, 1993
Summary
Neurodegenerative diseases involve excessive neuronal calcium. This study shows calbindin-D28k rapidly increases in Purkinje cells upon glutamate exposure, regulating calcium buffering independently of influx.
Area of Science:
- Neuroscience
- Cell Biology
- Neurodegenerative Diseases
Background:
- Excessive intracellular calcium is implicated in neurodegenerative disease pathophysiology.
- Excitatory amino acids induce neurotoxic increases in intracellular calcium, serving as a model for study.
Purpose of the Study:
- To investigate the role of calbindin-D28k in neuronal calcium regulation.
- To determine if calbindin-D28k expression changes in response to excitotoxic stimuli.
Main Methods:
- Utilized rat cerebellar slices superfused with glutamate or kainic acid.
- Measured calbindin-D28k levels in Purkinje cells.
- Investigated the effect of CNQX and calcium influx on calbindin-D28k response.
Main Results:
- Calbindin-D28k levels rapidly increased in Purkinje cells exposed to excitatory and excitotoxic concentrations of glutamate or kainic acid.
- This increase was reversible, reproducible, and blocked by CNQX.
- The calbindin-D28k upregulation was independent of calcium influx.
Conclusions:
- Calbindin-containing neurons can dynamically regulate their calcium buffering capacity.
- This regulation is triggered by specific agonists like glutamate.
- The mechanism of calbindin-D28k regulation does not involve cytosolic calcium increases.