Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock <italic style="font-style: italic">via</italic> Tau Protein Hyperphosphorylation in Depressed Rats<sup>△</sup>

Liu Wan-fu; Liu Chao

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Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△

中国医学科学杂志（英文版） 2015年30卷第2期页码：100-107

Original Articles | Updated：2024-04-10

- Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△
- Affiliations：
  
  1. 1Department of Anesthesiology, Fuzhou General Hospital of the People's Liberation Army Nanjing Military Region, Fujian 350025, China
  2. 2Department of Anesthesiology, Tianjin Chest Hospital, Tianjin 300222, China
- Author bio：
  
  *Corresponding author Tel: 86-18102022730, E-mail: liuchao74001@126.com
- Funds：
  
  △Supported by the National Natural Science Foundation (30972831) and the China Postdoctoral Science Foundation (2013M530880).
- DOI：
  中图分类号：
- 收稿日期：2015-01-03，
  
  网络出版日期：2015-04-20，
  
  纸质出版日期：2015-04
- Accepted：
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Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△[J]. 中国医学科学杂志（英文版）, 2015,30(2):100-107.

Liu Wan-fu, Liu Chao. Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△[J]. Chinese medical sciences journal, 2015, 30(2): 100-107.
Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△[J]. 中国医学科学杂志（英文版）, 2015,30(2):100-107. DOI：

Liu Wan-fu, Liu Chao. Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△[J]. Chinese medical sciences journal, 2015, 30(2): 100-107. DOI：

摘要

Abstract

Objective

To explore the possible neurophysiologic mechanisms of propofol and N-methyl-D- aspartate (NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs.

Methods

Models of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance

two intervention factors were included: electroconvulsive shock groups (with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal (ip) injection of saline

NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups (

=10 per group): ip injection of 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8

Ser202

in the hippocampus were determined by Western blot analysis.

Results

Propofol

MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats

as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol

but MK-801 had no significant effect on glutamic acid content. Levels of phosphorylated Tau protein p-AT8

Ser202

in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8

Ser202

levels induced by electroconvulsive shock.

Conclusion

Electroconvulsive shock might reduce learning-memory impairment caused by protein Tau hyperphosphorylation in depressed rats by down-regulating glutamate content.

关键词

Keywords

references

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Propofol Affects Different Human Brain Regions Depending on Depth of Sedation^△

Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats△

DOI：

摘要

Abstract

关键词

Keywords

references

Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats^△