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  • Title: Isoflurane inhibits neuronal Ca2+ channels through enhancement of current inactivation.
    Author: Kameyama K, Aono K, Kitamura K.
    Journal: Br J Anaesth; 1999 Mar; 82(3):402-11. PubMed ID: 10434825.
    Abstract:
    To help clarify the mechanisms by which volatile anaesthetics act on neuronal Ca2+ channel currents (IBa), the effects of isoflurane were studied on IBa in rat dorsal root ganglion (DRG) cells. Voltage-dependent IBa were pharmacologically subdivided into L-, N- and P/Q-types, and toxin-resistant IBa. At clinically relevant concentrations, isoflurane inhibited the L-, N- and P/Q-types, but not toxin-resistant IBa. The IC50 values for the L-, N- and P/Q-types were 0.7%, 1.3% and 3.0%, respectively (concentrations equivalent to 0.35, 0.68 and 1.46 mmol litre-1 in the aqueous phase). Isoflurane also produced initial transient augmentation of the N-type IBa. Isoflurane shifted the mid-point of the steady-state inactivation curve for the L-, N- and P/Q-type IBa towards negative potentials, and prolonged the time constant of current reactivation. We conclude that isoflurane inhibited L-, N- and P/Q-type IBa in rat DRG neurones by enhancing current inactivation and prolonging recovery time after inactivation. Transient augmentation of the N-type IBa may also form part of the overall actions of isoflurane in DRG neurones.
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