We studied the mechanisms of action of halothane and propofol on transmitter release and postsynaptic responses in both excitatory and inhibitory systems. Spontaneous miniature postsynaptic currents are ideal parameters for the analysis of anesthetic actions at both presynaptic and postsynaptic sites and postsynaptic receptor kinetics. Rat cortical neurons in primary culture were used to record these currents by the whole-cell patch clamp technique. Halothane at clinically relevant concentrations exerted a significant action on the inhibitory transmission by decreasing the frequency and prolonging the decay phase of spontaneous miniature inhibitory postsynaptic currents (mIPSCs) recorded in the presence of tetrodotoxin. Halothane also decreased the frequency of spontaneous miniature non-NMDA excitatory postsynaptic currents (mNN-EPSCs) without affecting their decay phase. Experiments using specific high voltage-gated calcium channel blockers indicated that halothane blocked N-type and P/Q-type calcium channels without effect on L-type calcium channels, thus leading to a decrease in the release of both excitatory and inhibitory transmitters. By contrast, the only effect of propofol was prolongation of the decay phase of mIPSCs. Halothane and propofol cause prolongation of mIPSCs, indicative of postsynaptic modulation without effect on mEPSCs. Halothane, but not propofol, reduces release of both excitatory and inhibitory transmitters via block of N- and P/Q-type calcium channels. The observed differences between halothane and propofol may be reflected in different clinical effects and usage.
|Original language||English (US)|
|Number of pages||2|
|Journal||Anesthesia and Resuscitation|
|State||Published - 2000|
ASJC Scopus subject areas
- Emergency Medicine
- Anesthesiology and Pain Medicine