The possibility that exposure to general anesthetics during early life results in long-term impairment of neural function attracted considerable interest over the past decade. Extensive laboratory data suggest that administration of these drugs during critical stages of central nervous system development can lead to cell death, impaired neurogenesis, and synaptic growth as well as cognitive deficits. These observations are corroborated by several recent human epidemiological studies arguing that such cognitive impairment might also occur in humans.
- Neonatal general anesthesia causes lasting alterations in excitatory and inhibitory synaptic transmission in the ventrobasal thalamus of adolescent female rats
- Mild hypothermia ameliorates anesthesia toxicity in the neonatal macaque brain
- Using animal models to evaluate the functional consequences of anesthesia during early neurodevelopment
- microRNA‐124 attenuates isoflurane‐induced neurological deficits in neonatal rats via binding to EGR1
- Hemin treatment protects neonatal rats from sevoflurane-induced neurotoxicity via the phosphoinositide 3-kinase/Akt pathway