Editorial  |   September 2020
Beyond Anesthesia Apoptosis: Wiring and Communication Matter!
Author Notes
  • From the Department of Anesthesiology and Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (V.J.-T.); and the Department of Anesthesiology, Pharmacology, Intensive Care and Emergency Medicine, University Hospitals of Geneva, Geneva, Switzerland (L.V.).
  • This editorial accompanies the article on p. 569.
    This editorial accompanies the article on p. 569.×
  • Accepted for publication June 17, 2020. Published online first on July 23, 2020.
    Accepted for publication June 17, 2020. Published online first on July 23, 2020.×
  • Address correspondence to Dr. Vutskits: laszlo.vutskits@hcuge.ch
Article Information
Editorial / Cardiovascular Anesthesia / Central and Peripheral Nervous Systems / Pharmacology
Editorial   |   September 2020
Beyond Anesthesia Apoptosis: Wiring and Communication Matter!
Anesthesiology 9 2020, Vol.133, 495-496. doi:https://doi.org/10.1097/ALN.0000000000003462
Anesthesiology 9 2020, Vol.133, 495-496. doi:https://doi.org/10.1097/ALN.0000000000003462
Although the potential human relevance remains controversial, animal data—from nematodes to nonhuman primates—published during the past two decades revealed that a wide assortment of general anesthetics can induce an extensive array of morphological and functional changes in the developing brain.1  Among the multitude of cellular responses triggered by general anesthetics, apoptosis or programmed cell death received the most attention. This entity is a commonly used endpoint of laboratory studies in the field of developmental anesthesia neurotoxicity, and its presence is often thought to be responsible for behavioral and cognitive dysfunctions later in life. Indeed, the prevailing view is that the initial neuronal destruction, as assessed by widespread neuroapoptotic activation, leads to ongoing disturbances in neuronal connectivity, synaptic plasticity, and interneuron dynamics, suggesting that the sequence of detrimental experimental outcomes stems from massive and widespread neuronal cell death.2  However, as of today, no causal relationship has been convincingly demonstrated between anesthesia-induced apoptosis and neural dysfunction. Therefore, an emerging plausible alternative is that early life anesthesia exposure–associated cognitive alterations, observed in a wide range of laboratory animals, may result from more subtle, yet long-lasting, changes in neuronal architecture and synaptic communication.