Abstract
Anesthetics evoke a stress-response, upregulating heat shock genes. This neuroprotective response to proteotoxic stress represents preconditioning, a process by which neuronal tissue, previously exposed to anesthetics, is protected against future insult. It presumes a sub-lethal injury, affecting protein unfolding. Our hypothesis is: preconditioning evokes molecular events that result in downstream changes that offer a selective advantage in terms of neuronal function. We focused on the neurobehavioral aspects which we neurophenotyped. Larval zebrafish were exposed to trifluoroethanol (TFE), an anesthetic mimetic, and tested for both individual and group behavioral markers of neuronal function. In bright/dark tests, we observed that TFE-exposed larvae spent more time in the dark area (typically an adult-like response) than control larvae. The response of TFE larvae to noise startle was directly opposite to that of controls. TFE larvae swam towards the source of the startle (into the bright zone), whereas control larvae swam away from the source of the startle (into the dark), typical of fear-response. The larvae also exhibited several differences in social behaviors, including synchronized schooling and shoaling behaviors. The TFE-group showed a greater number of synchronized events versus controls. The TFE-group also exhibited more shoaling events compared with controls. While the long-term effects have yet to be determined, these results shed light on the mechanism of anesthetic preconditioning. These complex zebrafish behaviors normally develop with age and therefore represent, in the TFE-exposed group, a pattern of accelerated maturation of neuronal function, which is the neurophenotype attributed to preconditioning.
Highlights
As the receptor targets of volatile anesthetics continue to be investigated, there is growing interest in the unintended consequences of anesthetics and the molecular targets that elicit these effects
Anesthetic preconditioning, which is analogous to ischemic preconditioning, is a process by which neuronal tissue previously exposed to volatile anesthetics exhibits a selective advantage, especially against future cellular insult
While the long-term effects have yet to be determined, the results of the current study may shed light on the mechanism of anesthetic preconditioning. These complex zebrafish behaviors normally develop with age and represent, in the TFE-exposed group, a pattern of accelerated maturation of neuronal function, which we attribute to the preconditioning effect of TFE
Summary
As the receptor targets of volatile anesthetics continue to be investigated, there is growing interest in the unintended consequences of anesthetics and the molecular targets that elicit these effects. Relevant questions include why select patient populations experience subtle adverse effects of anesthetics: individuals that are exposed to anesthetics very early in life may be at risk for later cognitive deficiencies [1], and some elderly patients may suffer sudden impaired quality of life following surgery—a process called post-operative cognitive dysfunction. The molecular mechanisms that are associated with these unintended detrimental effects of anesthetics remain poorly understood. Anesthetic preconditioning, which is analogous to ischemic preconditioning, is a process by which neuronal tissue previously exposed to volatile anesthetics exhibits a selective advantage, especially against future cellular insult. The precise molecular mechanism by which this occurs remains elusive
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