Desflurane impairs hippocampal learning on day 1 of exposure: A prospective laboratory study in rats

Abstract

Background: Quick and complete recovery of cognitive function after general anesthesia is desirable, particularly for working-age patients. Desflurane is less likely to have long-term effects than older-generation inhalational anesthetics, however, its short-term effects have not been fully investigated. Our objective was to elucidate the short-term effects of desflurane exposure on learning and memory in young adult rats. Methods: Seven-week old male Sprague-Dawley rats were exposed to air (control), or desflurane at 0.7 or 1.2 minimum alveolar concentration (MAC) for 2 h (day 0). The inhibitory avoidance (IA) test was performed on day 1 to delineate the effects on contextual learning. Separate groups of control and 1.2 MAC desflurane animals underwent the IA test on days 3 and 7 to examine the time-dependent changes. Because the IA test is known to be dependent on the long-term potentiation (LTP) of the hippocampus and the trafficking of the GluR1 subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor into the synapses, the effects of 1.2 MAC desflurane on these phenomena were evaluated on day 1. Results: Desflurane at 1.2 MAC, but not 0.7 MAC, significantly decreased the IA latencies on day 1 compared with the control (one-way ANOVA, F [2,48] = 5.974, P = 0.005, post hoc Tukey's, mean difference [95% confidence interval], control vs. 1.2 MAC, 168 [49.9 to 287], P = 0.004; control vs. 0.7 MAC, 67.5 [- 51.2 to 186], P = 0.362). The latencies were not affected on days 3 and 7 (day 3, control vs. desflurane, P = 0.861; day 7, control vs. desflurane, P > 0.999). Consistently, hippocampal LTP on day 1 was significantly suppressed in the desflurane group compared with the control group (P = 0.006). Moreover, immunoblotting analysis of synaptic GluR1 expression revealed that desflurane exposure significantly suppressed GluR1 delivery to the synapses after IA training. Conclusion: Exposure to a relatively high concentration of desflurane caused reversible learning and memory impairment in young adult rats associated with suppression of GluR1 delivery to the synapses in the hippocampus.