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General anesthetics are both neuroprotective and neurotoxic with unclear mechanisms. General anesthetics may control cell survival via their effects on autophagy by activation of type 1 inositol triphosphate receptor (InsP 3 R-1). DT40 or SH-SY5Y cells with only or over 99% expression of InsP 3 R-1 were treated with isoflurane or propofol. Cell viability was determined by MTT reduction or LDH release assays. Apoptosis was determined by measuring Caspase-3 or by TUNEL assay. Autophagy activity was determined by measuring LC3 II and P62. We evaluated mitochondrial integrity using MitoTracker Green and cytosolic ATP levels. Fura2-AM was used to measure the concentrations of cytosolic calcium ([Ca 2+ ] c ). Propofol significantly increased peak and integrated calcium response (P < 0.001) in cells with InsP 3 R-1 but not in cells with triple knockout of InsP 3 R. Both propofol and isoflurane increased autophagy induction (P < 0.05) in an mTOR- and InsP 3 R- activity dependent manner. Short exposure to propofol adequately activated InsP 3 -1 to provide sufficient autophagy for cytoprotection, while prolonged exposure to propofol induced cell apoptosis via impairment of autophagy flux through over activation of InsP 3 -1. Propofol damaged mitochondria and decreased cytosolic ATP. The effects of general anesthetics on apoptosis and autophagy are closely integrated; both are caused by differential activation of the type 1 InsP 3 R.

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General Anesthetics Regulate Autophagy via Modulating the Inositol 1,4,5-Trisphosphate Receptor: Implications for Dual Effects of Cytoprotection and Cytotoxicity