Abstract
BackgroundIsoflurane, a volatile anesthetic widely used clinically, has been implicated to be both neuroprotective and neurotoxic. The claim about isoflurane causing neural apoptosis remains controversial. In this study, we investigated the effects of isoflurane exposures on apoptotic and anti-apoptotic signals, cell proliferation and neurogenesis, and astroglial processes in young adult mouse brains.MethodsSixty 6-week-old mice were randomly assigned to four anesthetic concentration groups (0 as control and 0.6%, 1.3%, and 2%) with four recovery times (2 h and 1, 6, and 14 d) after 2-h isoflurane exposure. Immunohistochemistry measurements of activated caspase-3 and Bcl-xl for apoptotic and anti-apoptotic signals, respectively, glial fibrillary acidic protein (GFAP) and vimentin for reactive astrocytosis, doublecortin (Dcx) for neurogenesis, and BrdU for cell proliferation were performed.ResultsContrary to the previous conclusion derived from studies with neonatal rodents, we found no evidence of isoflurane-induced apoptosis in the adult mouse brain. Neurogenesis in the subgranule zone of the dentate gyrus was not affected by isoflurane. However, there is a tendency of reduced cell proliferation after 2% isoflurane exposure. VIM and GFAP staining showed that isoflurane exposure caused a delayed reduction of astroglial processes in the hippocampus and dentate gyrus.ConclusionTwo-hour exposure to isoflurane did not cause neuroapoptosis in adult brains. The delayed reduction in astroglial processes after isoflurane exposure may explain why some volatile anesthetics can confer neuroprotection after experimental stroke because reduced glial scarring facilitates better long-term neuronal recoveries.
Highlights
Volatile anesthetics have been implicated to be both neuroprotective and neurotoxic
It has been proposed that a prolonged exposure to volatile anesthetics is intrinsically neurotoxic and the observed protective effects are due to preconditioning, in which endogenous neuroprotective mechanisms are initiated by a limited exposure [6]
Unlike the situation in neonatal brains where apoptosis is a natural process of eliminating neurons that fail to establish synaptic connections, prolonged isoflurane exposure does not lead to apoptosis in young adult brains
Summary
Volatile anesthetics have been implicated to be both neuroprotective and neurotoxic. It has been proposed that a prolonged exposure to volatile anesthetics is intrinsically neurotoxic and the observed protective effects are due to preconditioning, in which endogenous neuroprotective mechanisms are initiated by a limited exposure [6]. Further investigations in cell cultures suggest that isoflurane preconditioning can protect astrocytes [7]. The anesthetic effects on astrocytes remain controversial. Isoflurane, a volatile anesthetic widely used clinically, has been implicated to be both neuroprotective and neurotoxic. The claim about isoflurane causing neural apoptosis remains controversial. We investigated the effects of isoflurane exposures on apoptotic and anti-apoptotic signals, cell proliferation and neurogenesis, and astroglial processes in young adult mouse brains
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