Although volatile anesthetic agents have been used clinically for many years, the mechanisms by which they act on the nervous system to produce anesthesia are not known. A possible site of action is the voltage-gated calcium-selective channel (Krnjevic and Puil, 1988). Accordingly, the action of the halogenated alkane anesthetic halothane on voltage-dependent Ca currents in neonatal rat sensory neurons was examined using whole-cell patch-clamp recordings. Halothane reversibly reduced the low-voltage-activated Ca current with an EC50 of about 100 microM. Similar effects were seen using a halogenated ether anesthetic (isoflurane) and in sensory neurons from adult rats. At higher concentrations, both halothane and isoflurane reduced the high-voltage- activated Ca current. Because low-voltage-activated Ca current. Because low-voltage-activated Ca current has been postulated to be involved in the control of neuronal excitability and bursting (Llinas, 1988), this block may explain some of the clinical actions of volatile anesthetics.