Inflammation causes deficits in learning and memory deficits through mechanisms that remain poorly understood. I will present evidence that memory loss associated with inflammation involves the same receptors that mediate the memory blocking properties of a variety of drugs, including anesthetics and benzodiazepines. Our results show that key pro-inflammatory cytokines including interleukin-1β (IL-1β) increase the activity of α5 subunit-containing γ- aminobutyric acid type A (α5GABAA) receptors. This increase in receptor activity reduces long-term potentiation, a synaptic correlate of memory, in hippocampal slices from wild-type mice. Further, IL-1β induced memory deficits were observed in WT but not Gabra5-/- mice. Collectively, the results show that α5GABAA receptor activity increases during inflammation and this increase is critical for inflammation-induced memory deficits.