Abstract: AIM: To study the effects of midazolam on the acetylcholine receptor (AChR) channels in rat superior cervical ganglion (SCG) neurons and the mechanisms of midazolam-induced hypotension.METHODS: Whole-cell patch-Clamp recordings were made from enzymatically isolated rat SCG neurons.RESULTS: At a holding potential (V_h) -60 mV, acetylcholine chloride evoked an inward current of rapid activation and then rapid desensitization decay, which was AChR channel currents, the half effective activation concentration (EC₅₀) was 39.65 μmol/L. Clinically relevant concentration of midazolam (0.3 μmol/L) inhibited the 200 μmol/L acetylcholine chloride-evoked macroscopic peak currents by 23.41% (P<0.05, n=6), enhanced the rates of desensitization from 45.59%±14.21% to 57.93%±13.74% (P<0.01, n=6), and these effects were dose dependent. Midazolam inhibited ACh-induced currents, but it did not alter the reversal potential of AChR channel. This inhibition was also voltage-independent at member potentials between -20 mV and -70 mV.CONCLUSION: Clinically relevant concentration of midazolam has significant inhibition on the AChR channel currents in rat sympathetic neurons; this inhibition is dos-dependent and voltage-independent, it is relevant to the desensitization of AChR channel.

Key words: Anesthesia, Midazolam, Patch-Clamp, AChR channel, Sympathetic ganglion