Research paperPropofol postsynaptically suppresses stellate neuron excitability in the entorhinal cortex by influencing the HCN and TREK-2 channels

- Propofol inhibited the firing rates of stellate neurons in the entorhinal cortex.
- The propofol-induced inhibition in entorhinal cortex reflected a postsynaptic effect.
- The inhibitory action of propofol was mediated by influence of HCN and TREK-2 channels.

The entorhinal cortex (EC) provides a majority of the excitatory inputs to the hippocampus and is part of the neural circuitry that is involved in memory formation. Although many studies have investigated the effects of propofol in the hippocampus, the function of propofol in the EC remains unclear. Here, using whole-cell patch clamp recordings, we found that propofol induced a postsynaptic outward current and dramatically suppressed the firing rates in the entorhinal stellate neurons, the axons of which form the perforant pathway and relay the main inputs to hippocampus. Propofol-induced inhibition in the EC was mediated by a dual ionic mechanism, including both HCN channel inhibition and TREK-2 channel activation, which form a subtype of two-pore-domain K+ channels. The inhibitory action of propofol observed in the EC might provide a mechanism for the anesthetic effect of propofol. Considering the crucial role of the EC in learning and memory, our findings may provide insight into the acute amnesic effect induced by propofol.