Halothane enhances exocytosis of [ 3 H]‐acetylcholine without increasing calcium influx in rat brain cortical slices

The effect of halothane on the release of [ 3 H]‐acetylcholine ([ 3 H]‐ACh) in rat brain cortical slices was investigated. Halothane (0.018 m M ) did not significantly affect the basal and the electrical field stimulation induced release of [ 3 H]‐ACh. However, halothane (0.063 m M ) significantly increased the basal release of [ 3 H]‐ACh and this effect was additive with the electrical field stimulation induced release of [ 3 H]‐ACh. The release of [ 3 H]‐ACh induced by 0.063 m M halothane was independent of the extracellular sodium and calcium ion concentration and was decreased by tetracaine, an inhibitor of Ca 2+ ‐release from intracellular stores or dantrolene, an inhibitor of Ca 2+ ‐release from ryanodine‐sensitive stores. Using 2‐(4‐phenylpiperidino)‐cyclohexanol (vesamicol), a drug that blocks the storage of ACh in synaptic vesicles, we investigated whether exocytosis of this neurotransmitter is involved in the effect of halothane. Vesamicol significantly decreased the release of [ 3 H]‐ACh evoked by halothane. It is suggested that halothane may cause a Ca 2+ release from intracellular stores that increases [ 3 H]‐ACh exocytosis in rat brain cortical slices.British Journal of Pharmacology (1999) 127 , 679–684; doi: 10.1038/sj.bjp.0702603