Propofol, a short‐acting general anesthetic, produces depression followed by rebound excitation overshoot of potentials evoked in the prepyriform (olfactory) cortex by stimulation of the lateral olfactory tract (LOT)

The role of the prepyriform cortex (PPC) in the anesthetic and subsequent excitatory state produced by propofol was studied in freely behaving rats bearing chronically implanted brain electrodes. Electrical stimulation of the PPC produces seizures more readily than stimulation of most other limbic areas, demonstrating the importance of the PPC in generating seizures in the rat. Propofol enhances the action of GABA on the GABAA receptor, producing an anesthetic state, accompanied by depression of potentials evoked in the hippocampus by stimulation of the dorsal perforant path and the PPC. This is followed by a rebound increase in amplitude and frequencies of the same potentials. Propofol abolished or reduced the amplitude of after‐potentials produced in the PPC by stimulation of the LOT, the principal input to the PPC. This was a typical anesthetic effect and was followed by a significant increase in the amplitude and occurrence of after‐potentials in the PPC. The latter was a typical excitatory effect. Chlordane, a GABA‐antagonist with seizure‐producing effects, had just the opposite effects of propofol during the anesthetic phase. Thus, the PPC is strongly affected by both GABA agonists like propofol and GABA antagonists like chlordane. In turn, they markedly influence seizure‐susceptibility. Supported by research funds from the University of California, Davis.