3 years ago

Anesthetic agents and neuronal autophagy. What we know and what we don't.

McQuillan, Shen, Hu, Xu
Numerous experimental data have demonstrated that neonatal animal exposure to commonly used anesthetic agents may cause neuronal death resulting in cognitive impairment. The underlying mechanism(s) remain elusive. Depending on the circumstances, autophagy may produce an effect that can be either protective or deleterious. Recent evidence demonstrates that this process can reduce the development of ethanol induced neurotoxicity and, as we know, ethanol has γ-Aminobutyric acid (GABA) agonist and N-methyl-D-aspartate (NMDA) antagonist characteristics similar to commonly used volatile anesthetic agents. Moreover, recent studies have found that general anesthesia causes long-term impairment of mitochondrial morphogenesis and synaptic transmission in the developing rat brain which is accompanied by enhancement of autophagic activity. Because of the mechanistic relationship between ethanol and a wide variety of anesthetic agents, as well as evidence of ethanol induced autophagy modulated neurotoxicity, we hypothesize that autophagy plays a role in general anesthetic induced neurotoxicity. It is known that anesthetic agents themselves may induce autophagy by modulating adenosine 5'-monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin (serine/threonine kinase) (MTOR) signaling, inducing oxidative stress and endoplasmic reticulum stress, disrupting intracellular calcium (Ca2+) homeostasis, and altering in BCL2 family proteins. This review explains the possible role of autophagy in the development of anesthetic related neurotoxicity from several aspects, including the relationship between anesthetic agents and neuronal autophagy, possible molecular and cellular mechanisms underlying general anesthetic agent induced activation of neuronal autophagy in the developing brain, and potential therapeutic approaches to modulate autophagic pathways. .

Publisher URL: http://doi.org/10.2174/0929867324666171009123605

DOI: 10.2174/0929867324666171009123605

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