ArticleNeurotoxicity research2022
Prenatal Isoflurane Exposure Induces Developmental Neurotoxicity in Rats: the Role of Gut Microbiota.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Gut‑brain axis in anesthesia and critical illness: Molecular crosstalk and its impact on delirium and outcome (Review).International journal of molecular medicine · 2026Review
- Up-regulation of miR-490-3p improves learning/memory disability of sevoflurane exposure by relieving neuroinflammation.Toxicology research · 2025Article
- Subsequent maternal sleep deprivation aggravates cognitive impairment by modulating hippocampal neuroinflammatory responses and synaptic function in maternal isoflurane-exposed offspring mice.Brain and behavior · 2024Article
- Article
- Modulation of gut microbiota with probiotics as a strategy to counteract endogenous and exogenous neurotoxicity.Advances in neurotoxicology · 2024Article
- The impact of electroacupuncture on anxiety-like behavior and gut microbiome in a mouse model of chronic restraint stress.Frontiers in behavioral neuroscience · 2023Article
- Research progress on molecular mechanisms of general anesthetic-induced neurotoxicity and cognitive impairment in the developing brain.Frontiers in neurology · 2022Review
- Differences in withdrawal symptoms, microglia activity, and cognitive functioning in rats exposed to continuous low-dose heroin in-utero.Neurotoxicology and teratologyArticle
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Authors and funding
6 authors at 2 institutions in 2 countries.
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Abstract
Fetal exposure to inhaled anesthetics, such as isoflurane, may lead to neurodevelopmental impairment in offspring. Yet, the mechanisms of prenatal isoflurane-induced developmental neurotoxicity have not been fully elucidated. Gut microbiota is a pivotal modulator of brain development and functions. While the antibiotic effect of isoflurane has been previously investigated, the relationship between prenatal isoflurane exposure and postnatal gut microbiota, brain biology, and behavior remains unknown. In the present study, we treated pregnant rats with 2% isoflurane for 4 h on gestational day 14. Their offspring were tested with novel object recognition task on postnatal day 28 (P28) to assess cognition. Fecal microbiome was assessed using 16S RNA sequencing. We also analyzed hippocampal expression of brain-derived neurotrophic factor (BDNF) in P28 rat brains. To further explore the role of gut microbiota on prenatal isoflurane-induced developmental neurotoxicity, we treated rats with mixed probiotics on P14 for 14 days and evaluated novel object recognition and hippocampal expression of BDNF on P28. Results indicate that prenatal exposure to isoflurane significantly decreased novel object recognition (novel object preference ratio: mean difference (MD) - 0.157; 95% confidence interval (CI) - 0.234 to - 0.080, P < 0.001) paralleled by diminished expression of hippocampal BDNF in juvenile rats. Prenatal exposure to isoflurane also significantly altered the diversity and composition of gut microbiota. Treatment with probiotics mitigated these changes in cognition (novel object preference ratio: isoflurane group vs. control group: MD - 0.177; 95% CI - 0.307 to - 0.047, P = 0.006; probiotic group vs. isoflurane group: MD 0.140; 95% CI 0.004 to 0.275, P = 0.042) and BDNF expression. Taken together, our findings suggest that gut dysbiosis may be involved in the pathogenesis of maternal isoflurane exposure-induced postnatal cognitive impairment. To determine the causal relationship between gut microbiota and cognition in prenatal anesthetic-induced developmental neurotoxicity, further studies are needed.
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