Effects of ketamine combined with electroconvulsive shock on inflammation and amyloid-beta peptide in hippocampus of depressive rats
10.11659/jjssx.01E017022
- VernacularTitle:氯胺酮联合电休克对抑郁样大鼠海马炎症及β淀粉样蛋白的影响
- Author:
Yi WANG
;
Xianlin ZHU
;
Zhenhua YANG
;
Zaiping WANG
;
Gang YE
- Keywords:
ketamine;
electroconvulsive shock;
memory;
inflammation;
amyloid-β
- From:
Journal of Regional Anatomy and Operative Surgery
2017;26(6):395-399
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ketamine combined with electroconvulsive shock (ECS) on inflammation and amyloid-beta peptide in hippocampus of depressive rats.Methods Chronic unpredictable mild stress (CUMS) was used to generate animal models of depression.Forty-eight adult male Sprague-Dawley rats were randomly divided into 4 groups (n=12):depression model group (group D),electroconvulsive shock group (group DE),ketamine combined with electroconvulsive shock group (group DKE),and ketamine group (group DK).Rats in group D received sham ECS treatment;rats in group DE received ECS treatment;rats in group DKE were given intraper-itoneal injection of ketamine (100 mg/kg) and then received ECS treatment;rats in group DK were given intraperitoneal injection of ketamine (100 mg/kg) and then received sham ECS treatment.Morris water maze was used to assess the memory abilities of rats.The expression levels of IL-1β and TNF-α were measured by real-time PCR.Enzyme-linked immunosorbent assays were used to detect the levels of soluble Aβ.Results Before the administration of ECS or ketamine treatment,there was no significant difference in the escape latencies and space exploration time between the 4 groups (P>0.05).After the ECS and ketamine treatment,rats of group DKE exhibited a shorter escape latencies and a longer space exploration time,and the expression of IL-1β and TNF-α mRNA were down-regulated while the concentration of Aβ1-40 and Aβ1-42 were increased compared with group DE with significant difference (P<0.05).Conclusion Ketamine can alleviate ECS-induced learning and memory impairments in depressive rats.This cognition-protecting effect of ketamine may be attributed to its suppression of ECS-induced neuroinflammation and decrease of the levels of soluble Aβ in the hippocampus of depressive rats.
