Arsenic exposure and glutamate-induced gliotransmitter release from astrocytes.

Abstract

The present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransmitter release. Primary astrocytes were exposed to 0, 2.5, 5, 10, 20 or 30 µM arsenite for 24 hours. Cell viability and morphological observations revealed that 5 µM arsenic exposure could induce cytotoxicity. Cells were then cultured in the presence of 0, 2.5, 5, or 10 µM arsenite for 24 hours and stimulated with 25 µM glutamate for 10 minutes. Results showed that [Ca2+]i in astrocytes exposed to 5 and 10 µM arsenite was significantly increased and levels of D-serine, γ-aminobutyric acid and glycine in cultures exposed to 2.5–10 µM arsenite were also increased. However, glutamate levels in the media were significantly increased only after treatment with 10 µM arsenite. In conclusion, our findings suggest that arsenic exposure may affect glutamate-induced gliotransmitter release from astrocytes and further disturb neuronal function.