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-bi nding protein, calbindin-D28k, increases rapidly in Purkinje cells of rat cerebellar slices superfused with excitatory and excitotoxic conce ntrations of glutamate or its analogue, kainic acid. The increase is r eversible and reproducible, is blocked by CNQX and is independent of C a2+ influx. These results indicate that calbindin containing neurones can regulate their Ca2+ buffering capacity in response to a specific a gonist and this regulation is not mediated by cytosolic calcium increa ses.