ArticleExperimental and therapeutic medicine2021
Repeated exposure to sevoflurane in neonatal rats impairs cognition in adulthood via the PKA-CREB-BDNF signaling pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.CNS neuroscience & therapeutics · 2026Review
- Review
- Deciphering sevoflurane-induced neurotoxicity: from isolated targets to intricate regulatory networks.Frontiers in neuroscience · 2025Review
- Inhibition of Adult Hippocampal Neurogenesis Plays a Role in Sevoflurane-Induced Cognitive Impairment in Aged Mice Through Brain-Derived Neurotrophic Factor/Tyrosine Receptor Kinase B and Neurotrophin-3/Tropomyosin Receptor Kinase C Pathways.Frontiers in aging neuroscience · 2022Article
- Neonatal Pain, Opioid, and Anesthetic Exposure; What Remains in the Human Brain After the Wheels of Time?Frontiers in pediatrics · 2022Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sevoflurane (Sev) anesthesia is widely used in pediatrics due to its low blood-gas partition coefficient and lack of pungency. However, Sev treatment may lead to cognitive dysfunction in later life. The current study administered Sev to neonatal rats to investigate the effects of Sev treatment on cognitive performance in adulthood. In total, 6-day-old rats received 3% Sev for 2 h daily for 3 consecutive days. The cognitive function of rats in adulthood was evaluated in 56-day-old rats by Morris water maze test. The hippocampal neuron morphology was observed by Nissl staining. Hippocampal brain-derived neurotrophic factor (BDNF) levels were measured by ELISA. The protein expression of protein kinase A (PKA), cAMP response element binding protein (CREB), phosphorylated-CREB (p-CREB) and BDNF in hippocampus were assessed by western blotting. The water maze results demonstrated that neonatal treatment with Sev resulted in a significant impairment of cognition in 56-day-old adult rats. Behavioral analysis revealed that Sev treatment increased latency to first pass the platform and decreased residence in target quadrants and across platform frequency compared with the control group in Morris water maze tests. Furthermore, compared with the control group, neonatal exposure to Sev reduced the number of neurons and the concentration of BDNF in the hippocampus, a brain region important for learning and memory. Additionally, Sev significantly decreased the expression of PKA, p-CREB, BDNF and the p-CREB/CREB ratio. Treatment with bucladesine, a selective PKA agonist, partially reversed the deleterious effects of Sev. In summary, the results indicated that PKA-CREB-BDNF signaling served an important role in the cognitive decline caused by neonatal exposure to Sev.
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