Summary of the effects of propofol on neuronal progenitor cell (NPC) proliferation and differentiation. Exposure to a clinically relevant concentration of propofol induces calcium release from the endoplasmic reticulum (ER) through the activation of the calcium channels, inositol 1,4,5-trisphosphate receptors (InsP₃R), and/or ryanodine receptors (RyR). This results in a moderate increase in the concentration of cytosolic calcium that stimulates NPC proliferation and neuronal and glial cell differentiation. These effects involve a nonautophagy mechanism. On the other hand, a prolonged exposure to a high concentration of propofol induces the overactivation of InsP₃Rs and/or RyRs on the ER membrane, thereby allowing the buildup of intracellular Ca²⁺. This elevated concentration of cytosolic calcium leads to excessive autophagy and the inhibition of NPC proliferation, which contributes to the propofol-mediated neurotoxicity. BAPTA-AM = bis-N,N,N',N'-tetraacetic acid-acetoxy methylester; IMP = inositol monophosphatase; IP₃ = inositol 1,4,5-trisphosphate; 3-MA = 3-methyladenine.