Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2012
Inhibition of α5 γ-Aminobutyric acid type A receptors restores recognition memory after general anesthesia.
General anesthetics cause cognitive deficits that persist much longer than would be expected on the basis of their pharmacokinetics. The cellular mechanisms underlying these postanesthetic cognitive deficits remain unknown. γ-Aminobutyric acid type A (GABA(A)) receptors are principal targets for most anesthetics. In particular, the α5GABA(A) receptor subtype has been implicated in acute memory blockade during anesthesia and memory deficits in the early postoperative period. We first sought to determine whether working memory and short-term recognition memory are impaired after isoflurane anesthesia. The second aim of the study was to determine whether memory deficits after isoflurane can be reversed by inhibiting α5GABA(A) receptors. We also sought to determine whether the expression of α5GABA(A) receptors is necessary for the development of memory dysfunction after isoflurane. Lastly, the effect of sevoflurane on memory was studied. ⋯ Inhalational anesthetics cause deficits in anterograde recognition memory. This proof-of-concept study shows that α5GABA(A) receptors are necessary for the development of postanesthetic deficits in recognition memory and that these receptors can be targeted to restore memory even after the anesthetic has been eliminated.