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.
- Cell cycle activation contributes to isoflurane-induced neurotoxicity in the developing brain and the protective effect of CR8.
- Protective Effects of Xenon on Propofol-Induced Neurotoxicity in Human Neural Stem Cell-Derived Models.
- Neonatal exposure to propofol affects interneuron development in the piriform cortex and causes neurobehavioral deficits in adult mice.
- The expression of glucose transporters and mitochondrial division and fusion proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity.
- Inhibition of microRNA-375 ameliorated ketamine-induced neurotoxicity in human embryonic stem cell derived neurons.