Send to

Choose Destination
See comment in PubMed Commons below
Can J Anaesth. 2011 Feb;58(2):167-77. doi: 10.1007/s12630-010-9428-8. Epub 2010 Dec 23.

Inhibition of learning and memory by general anesthetics.

Author information

Department of Anesthesia, University of Toronto, Rm. 3318, Medical Sciences Building, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.



Today's general anesthetics were developed empirically according to their ability to produce memory blockade, analgesia, immobility, and unconsciousness. Thus, a major outstanding question remains: How do anesthetics produce their desirable behavioural end points at the molecular level? Understanding the mechanisms underlying memory blockade is of particular importance, because some patients experience the unexpected recall of events during anesthesia while others experience persistent memory deficits in the postoperative period. This review provides a brief summary of the acute memory-blocking properties of general anesthetics and the neuronal substrates that most likely contribute to memory loss.


Studies in human volunteers and laboratory animals have shown that the memory-blocking properties of general anesthetics depend on the specific drug, the dose, the type of memory, and the experimental paradigm, as well as the species and age of the experimental subject. The cellular substrates of memory blockade include an increase in neuronal inhibition by γ-aminobutyric acid subtype A receptors, a decrease in excitatory glutamatergic neurotransmission, and alterations in synaptic plasticity.


Anesthetics target different receptors and brain regions to modify the various forms of memory. In the hippocampus, extrasynaptic γ-aminobutyric acid subtype A receptors may play a particularly important role. Knowledge regarding the molecular basis of memory blockade may help to address memory disorders associated with the anesthetic state.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center