CYTOPLASMIC CALCIUM BUFFER, CALBINDIN-D28K, IS REGULATED BY EXCITATORY AMINO-ACIDS

EXCESSIVE intracellular calcium in neurones is thought to underlie the pathophysiology of several neurodegenerative diseases. An extensively studied animal model is the neurotoxic increases in intracellular Ca2+ induced by excitatory amino acid. We report here that the calcium-binding protein, calbindin-D28k, increases rapidly in Purkinje cells of rat cerebellar slices superfused with excitatory and excitotoxic concentrations of glutamate or its analogue, kainic acid. The increase is reversible and reproducible, is blocked by CNQX and is independent of Ca2+ influx. These results indicate that calbindin containing neurones can regulate their Ca2+ buffering capacity in response to a specific agonist and this regulation is not mediated by cytosolic calcium increases.