PMID- 30118751
OWN - NLM
STAT- MEDLINE
DCOM- 20190329
LR  - 20190329
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 388
DP  - 2018 Sep 15
TI  - Aberrant Amygdala-dependent Fear Memory in Corticosterone-treated Mice.
PG  - 448-459
LID - S0306-4522(18)30542-6 [pii]
LID - 10.1016/j.neuroscience.2018.08.004 [doi]
AB  - Anxiety disorder is a major psychiatric disorder characterized by fear, worry, 
      and excessive rumination. However, the molecular mechanisms underlying neural 
      plasticity and anxiety remain unclear. Here, we utilized a mouse model of 
      anxiety-like behaviors induced by the chronic administration of corticosterone 
      (CORT) to determine the exact mechanism of each region of the fear circuits in 
      the anxiety disorders. Chronic CORT-treated mice showed a significant increase in 
      anxiety-related behaviors as assessed by the elevated plus maze, light-dark, 
      open-field, and marble-burying tasks. In addition, chronic CORT-treated mice 
      exhibited abnormal amygdala-dependent tone-induced fear memory but normal 
      hippocampus-dependent contextual memory. Consistent with amygdala 
      hyperactivation, chronic CORT-treated mice showed significantly increased numbers 
      of c-Fos-positive cells in the basolateral amygdala (BLA) after tone stimulation. 
      Long-term potentiation (LTP) was markedly enhanced in the BLA of chronic 
      CORT-treated mice compared to that of vehicle-treated mice. Immunoblot analyses 
      revealed that autophosphorylation of Ca(2+)/calmodulin-dependent protein kinase 
      (CaMK) IIalpha at threonine 286 and phosphorylation of cyclic-adenosine-monophosphate 
      response-element-binding protein (CREB) at serine 133 were markedly increased in 
      the BLA of chronic CORT-treated mice after tone stimulation. The protein and mRNA 
      levels of brain-derived neurotrophic factor (BDNF) also significantly increased. 
      Our findings suggest that increased CaMKII activity and synaptic plasticity in 
      the BLA likely account for the aberrant amygdala-dependent fear memory in chronic 
      CORT-treated mice.
CI  - Copyright (c) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Inagaki, Ryo
AU  - Inagaki R
AD  - Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku 
      University, Japan. Electronic address: ryo.inagaki.r5@dc.tohoku.ac.jp.
FAU - Moriguchi, Shigeki
AU  - Moriguchi S
AD  - Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku 
      University, Japan. Electronic address: shigeki@m.tohoku.ac.jp.
FAU - Fukunaga, Kohji
AU  - Fukunaga K
AD  - Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku 
      University, Japan. Electronic address: kfukunaga@m.tohoku.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180816
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Bdnf protein, mouse)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Creb1 protein, mouse)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 2.7.11.17 (Camk2a protein, mouse)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Amygdala/*metabolism
MH  - Animals
MH  - Anxiety/metabolism
MH  - Auditory Perception/physiology
MH  - Behavior, Animal/physiology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism
MH  - Corticosterone/administration & dosage/*metabolism
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Fear/*physiology
MH  - Long-Term Potentiation/physiology
MH  - Male
MH  - Memory/*physiology
MH  - Mice, Inbred C57BL
MH  - Phosphorylation
MH  - RNA, Messenger/metabolism
OTO - NOTNLM
OT  - CaMKII
OT  - amygdala
OT  - corticosterone
OT  - fear memory
OT  - long-term potentiation
EDAT- 2018/08/18 06:00
MHDA- 2019/03/30 06:00
CRDT- 2018/08/18 06:00
PHST- 2017/12/07 00:00 [received]
PHST- 2018/08/02 00:00 [revised]
PHST- 2018/08/06 00:00 [accepted]
PHST- 2018/08/18 06:00 [pubmed]
PHST- 2019/03/30 06:00 [medline]
PHST- 2018/08/18 06:00 [entrez]
AID - S0306-4522(18)30542-6 [pii]
AID - 10.1016/j.neuroscience.2018.08.004 [doi]
PST - ppublish
SO  - Neuroscience. 2018 Sep 15;388:448-459. doi: 10.1016/j.neuroscience.2018.08.004. 
      Epub 2018 Aug 16.