Effects of neurotransmitters on calcium efflux from cultured glioma cells

Abstract
The effects of various neurotransmitters and cyclic nucleotides on 45Ca2+ efflux in cultured human glioma cells were investigated. Glutamate and glycine, but not GABA, stimulated 45Ca2+ release from the cells. Stimulation of beta‐adrenergic receptors but not alpha‐adrenergic receptors also increased 45Ca2+ efflux. Cholinergic receptor stimulation by carbachol had the same effect. The stimulatory effect of carbachol was abolished in the presence of either atropine or hexamethonium. C‐AMP and c‐GMP increased the 45Ca2+ efflux, suggesting that these agents are involved in the transmitter‐stimulated release of 45Ca2+ from the cells. Kinetic analysis of the efflux revealed four calcium compartments. The carbachol‐stimulated efflux represented a net release of calcium and could be ascribed to the slowest compartment. The physiological role of the transmitter‐stimulated calcium release is discussed in terms of calcium‐regulated stimulus‐response coupling in glial‐neural interaction during excitation.