Since 1999, a large body of evidence from various animal models indicates a link between anesthesia exposure in early stage of life and subsequent neurodevelopmental impairments; namely, almost all commonly used intravenous and inhalational anesthetics, including gamma-aminobutyric acid agonists and N-methyl-D-aspartate antagonists, can induce dose- and age-dependent neuronal apoptosis and death in vitro. Moreover, abundant data from nematodes to primate animals have shown a variety of anatomic and neurodevelopmental sequelae from anesthesia exposure in young animals. In the rodents, the most prominent manifestations of anesthesia-induced developmental neurotoxicity (AIDN) are often observed at post-natal day 7, which is the peak period for synaptogenesis. In animal models, both single and multiple anesthesia exposures can affect neurodevelopment. Also, the duration and timing of anesthesia exposure are the important influencing factors of AIDN. Alarmingly, these neurotoxic effects by neonatal exposure to anesthesia may result in the long-term detrimental functional outcomes in later childhood or adulthood, such as deficits in memory, learning, attention, and motor function.
- Sevoflurane diminishes neurogenesis and promotes ferroptosis in embryonic prefrontal cortex via inhibiting nuclear factor-erythroid 2-related factor 2 expression.
- Neonatal Anesthesia and Oxidative Stress.
- LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497-5p to upregulate NLRX1.
- Downregulation of HOTAIR reduces neuronal pyroptosis by targeting miR-455-3p/NLRP1 axis in propofol-treated neurons in vitro.
- MiRNA-384-5p targets GABRB1 to regulate ketamine-Induced Neurotoxicity in Neurons.