Isoflurane does not cause neuroapoptosis but reduces astroglial processes in young adult mice

Sixty 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.Contrary 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.Two-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.Volatile anesthetics have been implicated to be both neuroprotective and neurotoxic. Several studies have shown that volatile anesthetics can reduce neurological damage from ischemia by reducing glutamate release, blocking glutamate receptors, enhancing hyperpolarization by GABA, increasing anti-apoptotic bcl-2 levels, activating p38 mitogen-activated protein kinases, and inducing neurogenesis [1-3]. Conversely, isoflurane has also been implicated in post-anesthesia cognitive decline, possible interaction and exacerbation of the accumulation of amyloid-β plaques found in Alzheimer's disease, and apoptosis in the developing brain [4,5].It has been proposed that a prolonged exposure to volatile ane