| First Author | Li Y | Year | 2019 |
| Journal | Brain Res | Volume | 1710 |
| Pages | 188-198 | PubMed ID | 30529655 |
| Mgi Jnum | J:277793 | Mgi Id | MGI:6295554 |
| Doi | 10.1016/j.brainres.2018.12.010 | Citation | Li Y, et al. (2019) Sevoflurane-induced learning deficits and spine loss via nectin-1/corticotrophin-releasing hormone receptor type 1 signaling. Brain Res 1710:188-198 |
| abstractText | In recent years, the neurotoxicity of general anesthetics in the developing brain has been studied and raised great concern as a major health issue to the public and physicians. Sevoflurane inhalation may induce neurotoxicity expressed as memory and learning impairment in young animals. In the current study, we investigated the role of nectin-1 and corticotrophin-releasing hormone receptor type 1 (CRHR1) in sevoflurane-induced learning deficits and dendritic spines loss in neonatal mice. Neonatal mice (P7) were treated with 3% sevoflurane with 60% O2 or 60% O2 for 6h. Cognitive function was evaluated by Y Maze, Object recognition test, and Morris Water Maze. Hippocampal nectin-1 and L-afadin expression assessed using western blot analysis. The dendritic spines morphology of the hippocampus was determined using Golgi impregnation on 7 d and 2months old. Sevoflurane exposed to neonatal mice decreased hippocampal nectin-1 levels from 1h to 2months after sevoflurane inhalation and attenuated working and spatial memory and spinal number in adulthood, which could be reversed by nectin-1 overexpression and CRHR1 antagonist Antalarmin. Nectin-1 knockdown caused spatial learning deficits and dendritic spine loss and lower L-afadin protein expression. Sevoflurane-induced nectin-1 and L-afadin expression decrease was mediated by CRHR1 signaling in the hippocampus. This information can be used to develop targeted intervention aimed at decreasing the neurotoxicity of sevoflurane inhalation. |
