Stellate ganglion block alleviates hippocampal excitotoxicity and spatial learning memory impairment in sleep-deprived rats
10.16557/j.cnki.1000-7547.2024.04.004
- VernacularTitle:星状神经节阻滞缓解睡眠剥夺大鼠海马兴奋性毒性与空间学习记忆损伤
- Author:
Biqiong ZHENG
1
,
2
;
Jiaqi LI
;
Changyi LIU
;
Rujie ZHENG
;
Shuhui HU
Author Information
1. 福建医科大学附属第一医院麻醉科,福州 350004
2. 福建医科大学附属第一医院滨海院区国家区域医疗中心麻醉科,福州 350212
- Keywords:
rapid eye movement sleep deprivation(RSD);
stellate ganglion block(SGB);
spatial learning memory function;
excitatory amino acids;
rat
- From:
Chinese Journal of Neuroanatomy
2024;40(4):429-434
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the protective effect and possible mechanism of stellate ganglion block(SGB)on spatial learning memory function impairment in rapid eye movement sleep deprived(RSD)rats.Methods:Thirty-two rats were randomly assigned to Control group,RSD group,SGB group,and rapid eye movement sleep deprivation with stellate ganglion block intervention(RSD+SGB)group.The rats in RSD group and RSD+SGB group were modeled by modified multi-platform method(MMPM),and the rats in SGB group and RSD+SGB group were intervened by the SGB method.Morris water maze(MWM)was selected to evaluate the spatial learning and memory functions of rats in each group,and the expression levels of glutamate(Glu)and aspartate(Asp)in hippocampal tissues of rats in each group were detected by colorimetric assay,and the expression levels of N-methyl-D-aspartate receptor 1(NR1)and caspase-3 in hippocampal tissues of rats in each group were detected by Western Blot.Results:Compared with the RSD group,rats in RSD+SGB group had a significantly shorter escape latency after SGB intervention(P＜0.05),while the number of passes through the original platform position and the percentage of target quadrant time were significantly in-creased(P＜0.05);at the same time,the hippocampal tissues'expression levels of Glu,Asp,NR1,and caspase-3 were all significantly reduced(P＜0.05).Conclusion:SGB protects against RSD-induced impairment of spatial learn-ing memory capacity by reducing hippocampal tissue excitotoxicity and apoptosis induced by excitatory amino acid hyper-activation in RSD rats.
