Sevoflurane induces temporary spatial working memory deficits and synaptic ultrastructure impairments in the hippocampus of neonatal rats

G.-Y. Sun, K. Xie, Z.-Y. Sun, M.-Y. Sun, N. Li

Department of Anesthesiology, the Second Hospital of Shandong University, Jinan, China. lining252252@126.com

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• Pharmacology

OBJECTIVE: Exposure to volatile anesthetics in neonatal rats could induce neurotoxicity, learning deficits and abnormal social behaviors. The aim of this study is to investigate the potential neurotoxicity induced by sevoflurane.

MATERIALS AND METHODS: Postnatal day 7 (P7) Sprague-Dawley (SD) rats were continuously exposed to 2% sevoflurane plus 40% oxygen/air for 2 h. We used Morris water maze (MWM) to examine subsequent neurobehavioral performance. Transmission electron microscopy (TEM) was used to observe the histopathological changes in the hippocampus.

RESULTS: Neonatal exposure to 2% sevoflurane for 2 hours impaired short-term spatial working memory but not reference memory at P25. It induced synaptic ultrastructure impairments in the CA3 region of hippocampal, including fewer numbers of synapses, thinner thickness of postsynaptic dense, broader synaptic cleft width and smaller synaptic curvature. Our results also showed that all synaptic ultrastructure impairments and neurocognitive deficits had almost completely recovered at P53.

CONCLUSIONS: We showed that a single sevoflurane exposure to neonatal rats led to temporary spatial working memory deficits. It might be associated with synaptic ultrastructure impairments in the CA3 region of the hippocampus, including fewer numbers of synapses, thinner thickness of PSD and broader synaptic cleft width. Fortunately, all the neurotoxicity and neurocognitive deficits were reversible.

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