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.
- Prenatal Exposure to General Anesthesia Drug Esketamine Impaired Neurobehavior in Offspring.
- Needle in a Haystack: Localising the Long-Term Neuronal Changes from Early-Life Exposure to General Anaesthesia.
- Toll-Like Receptor 4 Deficiency Ameliorates Propofol-Induced Impairments of Cognitive Function and Synaptic Plasticity in Young Mice.
- Whole-Brain Characterization of Apoptosis after Sevoflurane Anesthesia Reveals Neuronal Cell Death Patterns in the Mouse Neonatal Neocortex.
- Apamin, an SK2 Inhibitor, Attenuated Neonatal Sevoflurane Exposures Caused Cognitive Deficits in Mice through the Regulation of Hippocampal Neuroinflammation.