ArticleNeurotoxicology and teratology2017
Carbon monoxide incompletely prevents isoflurane-induced defects in murine neurodevelopment.
Article in Neurotoxicology and teratology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 9 citations in OpenAlex.
- Exogenous Carbon Monoxide Produces Rapid Antidepressant- and Anxiolytic-Like Effects.Frontiers in pharmacology · 2021Article
- Data on the effect of sex on the size, cellular content, and neuronal density of the developing brain in mice exposed to isoflurane and carbon monoxide.Data in brief · 2017Article
- Neurotoxicity of anesthetics: Mechanisms and meaning from mouse intervention studies.Neurotoxicology and teratologyReview
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7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundCommonly used anesthetics have been shown to disrupt neurodevelopment in preclinical models. It has been proposed that such anesthesia-induced neurotoxicity is mediated by apoptotic neurodegeneration in the immature brain. Low dose carbon monoxide (CO) exerts cytoprotective properties and we have previously demonstrated that CO inhibits isoflurane-induced apoptosis in the developing murine brain. Here we utilized anti-apoptotic concentrations of CO to delineate the role of apoptotic neurodegeneration in anesthesia-induced neurotoxicity by assessing the effect of CO on isoflurane-induced defects in neurodevelopment.
methodsC57Bl/6 mouse pups underwent 1-hour exposure to 0ppm (air), 5ppm, or 100ppm CO in air with or without isoflurane on postnatal day 7. Cohorts were evaluated 5-7weeks post exposure with T-maze cognitive testing followed by social behavior assessment. Brain size, whole brain cellular content, and neuronal density in primary somatosensory cortex and hippocampal CA3 region were measured as secondary outcomes 1-week or 5-7weeks post exposure along with 7-day old, unexposed controls.
resultsIsoflurane impaired memory acquisition and resulted in abnormal social behavior. Low concentration CO abrogated anesthetic-induced defects in memory acquisition, however, it also resulted in impaired spatial reference memory and social behavior abnormalities. Changes in brain size, cellular content, and neuronal density over time related to the age of the animal and were unaffected by either isoflurane or CO.
conclusionsAnti-apoptotic concentrations of CO incompletely prevented isoflurane-induced defects in neurodevelopment, lacked concentration-dependent effects, and only provided protection in certain domains suggesting that anesthesia-related neurotoxicity is not solely mediated by activation of the mitochondrial apoptosis pathway.
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