PMID- 25533726
OWN - NLM
STAT- MEDLINE
DCOM- 20160303
LR  - 20181202
IS  - 1438-8359 (Electronic)
IS  - 0913-8668 (Linking)
VI  - 29
IP  - 4
DP  - 2015 Aug
TI  - Sevoflurane attenuates stress-enhanced fear learning by regulating hippocampal 
      BDNF expression and Akt/GSK-3beta signaling pathway in a rat model of post-traumatic 
      stress disorder.
PG  - 600-8
LID - 10.1007/s00540-014-1964-x [doi]
AB  - PURPOSE: Post-traumatic stress disorder (PTSD) is a psychiatric disease that may 
      occur after intense psychological trauma or physiological stress. Accumulating 
      evidence suggests that brain-derived neurotrophic factor (BDNF) and the 
      serine/threonine kinase (Akt)/glycogen synthase kinase-3beta (GSK-3beta) signaling 
      pathway are critically involved in brain plasticity, including 
      hippocampal-dependent learning and memory, while sevoflurane impairs memory 
      processing. Thus, we hypothesized that sevoflurane can suppress fear learning by 
      regulating the expression of BDNF and the Akt/GSK-3beta signaling pathway in a rat 
      model of PTSD. METHOD: Rats were exposed to sevoflurane during or after a 15 
      foot-shock stressor. Thereafter, rats were subjected to a single foot-shock in a 
      totally different environment. The fear response was recorded in response to the 
      15 foot-shock and the single foot-shock environments. In another set of 
      experiments, the brain tissue was harvested and subjected to biochemistry 
      studies. RESULTS: Our data suggested that increasing sevoflurane concentrations 
      decreased stress-enhanced fear learning (SEFL) when given during but not after 
      the stressor. Furthermore, administration of lithium chloride (100 mg/kg, 
      intraperitoneally) 30 min before the contextual fear conditioning reversed the 
      inhibitory effect of 0.8 % sevoflurane on SEFL as well as phosphorylated (p)-Akt, 
      p-GSK-3beta and BDNF expressions. CONCLUSION: Our data suggested that increasing 
      sevoflurane administration during but not after the stressor can impair SEFL in a 
      rat model of PTSD, which may be due, at least in part, to the regulation of 
      hippocampal BDNF expression and the Akt/GSK-3beta signaling pathway.
FAU - Chen, Chunlong
AU  - Chen C
AD  - Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing 
      University, 305 East Zhongshan Road, Nanjing, 210002, China.
FAU - Ji, Muhuo
AU  - Ji M
FAU - Xu, Qian
AU  - Xu Q
FAU - Zhang, Yao
AU  - Zhang Y
FAU - Sun, Qian
AU  - Sun Q
FAU - Liu, Jian
AU  - Liu J
FAU - Zhu, Sihai
AU  - Zhu S
FAU - Li, Weiyan
AU  - Li W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141223
PL  - Japan
TA  - J Anesth
JT  - Journal of anesthesia
JID - 8905667
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Methyl Ethers)
RN  - 38LVP0K73A (Sevoflurane)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - EC 2.7.11.1 (GSK3B protein, human)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.1 (Gsk3b protein, rat)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Disease Models, Animal
MH  - Fear/*drug effects
MH  - Glycogen Synthase Kinase 3/metabolism
MH  - Glycogen Synthase Kinase 3 beta
MH  - Hippocampus/*drug effects
MH  - Male
MH  - Methyl Ethers/*pharmacology
MH  - Phosphorylation/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sevoflurane
MH  - Signal Transduction/drug effects
MH  - Stress Disorders, Post-Traumatic/*drug therapy
EDAT- 2014/12/24 06:00
MHDA- 2016/03/05 06:00
CRDT- 2014/12/24 06:00
PHST- 2014/10/04 00:00 [received]
PHST- 2014/12/10 00:00 [accepted]
PHST- 2014/12/24 06:00 [entrez]
PHST- 2014/12/24 06:00 [pubmed]
PHST- 2016/03/05 06:00 [medline]
AID - 10.1007/s00540-014-1964-x [doi]
PST - ppublish
SO  - J Anesth. 2015 Aug;29(4):600-8. doi: 10.1007/s00540-014-1964-x. Epub 2014 Dec 23.