The general anaesthetic propofol prevents cerebrocortical potentiation in neocortical mouse brain slices

Propofol is well known to cause amnesia independent of its sedative effect. Memory consolidation processes in the hippocampus have been proposed as a target - however the neural substrates for propofol's amnesic actions remain understudied and poorly described. In particular, the potential role of the cerebral cortex has not been investigated. As an in vitro experimental model of cortical memory consolidation, potentiated cerebral cortex evoked re-sponses were generated in mouse neocortical slices using high frequency (20 Hz) stimulation to layer IV cortical grey matter or subcortical white matter. In separate experiments, slices were pretreated with propofol at two concentrations, 2 mu g/mL and 4 mu g/mL, to determine the effect of clinically relevant propofol levels on the potentiation response. Only grey matter stimulation induced a significant and lasting increase in cortical evoked potential amplitude in the drug-free condition. Propofol at 2 mu g/mL completely inhibited cortical evoked response potentiation, while the 4 mu g/mL concentration caused a small but significant depressant effect consequent to the high frequency stimulation. These findings support the hypothesis that propofol disrupts memory consolidation and actively facilitates memory decay in the cerebral cortex. The results further highlight the importance of the cerebral cortex in the early phase of long term memory consolidation.

Automated summary

Propofol disrupts memory consolidation and actively facilitates memory decay in the cerebral cortex.