Abstract
The cellular target site(s) for anaesthetic action remain unclear. In rat striatal slices we have previously demonstrated that K +-evoked noradrenaline (NA) and dopamine (DA) release is mediated predominantly via P/Q-type voltage sensitive Ca 2+ channels (VSCC). Using this model of Ca 2+ dependent transmitter release we have evaluated the effects of anaesthetic and non-anaesthetic barbiturates. Rat brain striatal slices were incubated in the absence and presence of barbiturate for 10 min at 37°C. The slices were then incubated for 6 min with 40 mM KCl. All anaesthetic barbiturates produced a concentration-dependent inhibition of K +-evoked NA and DA release. Non-anaesthetic barbiturate, barbituric acid was ineffective. The pIC 50 for NA and DA release (thiopental: 4.90±0.13 and 5.00±0.10, pentobarbital: 4.39±0.07 and 4.43±0.14, phenobarbital: 3.85±0.08 and 3.59±0.10, respectively) correlated with lipid solubility (NA: r 2=0.999, DA: r 2=0.987). We therefore suggest that barbiturates inhibit catecholamine release via an interaction with P/Q VSCC further implicating this channel in anaesthetic action.
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