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.
- Neonatal Isoflurane Anesthesia or Disruption of Postsynaptic Density-95 Protein Interactions Change Dendritic Spine Densities and Cognitive Function in Juvenile Mice.
- Autophagic Network Analysis of the Dual Effect of Sevoflurane on Neurons Associated with GABARAPL1 and 2.
- Effects of ketamine on neurogenesis, extracellular matrix homeostasis and proliferation in hypoxia-exposed HT22 murine hippocampal neurons.
- LncRNA Rik-203 Contributes to Sevoflurane Induced Neurotoxicity?
- Upregulation of miR-215 attenuates propofol-induced apoptosis and oxidative stress in developing neurons by targeting LATS2.