PMID- 24849362
OWN - NLM
STAT- MEDLINE
DCOM- 20140711
LR  - 20211021
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 34
IP  - 21
DP  - 2014 May 21
TI  - Involvement of BDNF signaling transmission from basolateral amygdala to 
      infralimbic prefrontal cortex in conditioned taste aversion extinction.
PG  - 7302-13
LID - 10.1523/JNEUROSCI.5030-13.2014 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related 
      kinase receptor B (TrkB), play a critical role in memory extinction. However, the 
      detailed role of BDNF in memory extinction on the basis of neural circuit has not 
      been fully understood. Here, we aim to investigate the role of BDNF signaling 
      circuit in mediating conditioned taste aversion (CTA) memory extinction of the 
      rats. We found region-specific changes in BDNF gene expression during CTA 
      extinction. CTA extinction led to increased BDNF gene expression in the 
      basolateral amygdala (BLA) and infralimbic prefrontal cortex (IL) but not in the 
      central amygdaloid nucleus (CeA) and hippocampus (HIP). Moreover, blocking BDNF 
      signaling or exogenous microinjection of BDNF into the BLA or IL could disrupt or 
      enhance CTA extinction, which suggested that BDNF signaling in the BLA and IL is 
      necessary and sufficient for CTA extinction. Interestingly, we found that 
      microinjection of BDNF-neutralizing antibody into the BLA could abolish the 
      extinction training-induced BDNF mRNA level increase in the IL, but not vice 
      versa, demonstrating that BDNF signaling is transmitted from the BLA to IL during 
      extinction. Finally, the accelerated extinction learning by infusion of exogenous 
      BDNF in the BLA could also be blocked by IL infusion of BDNF-neutralizing 
      antibody rather than vice versa, indicating that the IL, but not BLA, is the 
      primary action site of BDNF in CTA extinction. Together, these data suggest that 
      BLA-IL circuit regulates CTA memory extinction by identifying BDNF as a key 
      regulator.
CI  - Copyright (c) 2014 the authors 0270-6474/14/347302-12$15.00/0.
FAU - Xin, Jian
AU  - Xin J
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and.
FAU - Ma, Ling
AU  - Ma L
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and Department of Clinical Laboratory, Second Hospital of Shandong 
      University, Jinan, Shandong 250033, P.R. China.
FAU - Zhang, Tian-Yi
AU  - Zhang TY
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and.
FAU - Yu, Hui
AU  - Yu H
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and.
FAU - Wang, Yue
AU  - Wang Y
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and.
FAU - Kong, Liang
AU  - Kong L
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and.
FAU - Chen, Zhe-Yu
AU  - Chen ZY
AD  - Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. 
      China, and zheyuchen@sdu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Antibodies)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Carbazoles)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Indole Alkaloids)
RN  - 97161-97-2 (staurosporine aglycone)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
CIN - J Neurosci. 2014 Sep 17;34(38):12617-8. PMID: 25232100
MH  - Amygdala/drug effects/*physiology
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Avoidance Learning/drug effects/*physiology
MH  - Brain-Derived Neurotrophic Factor/genetics/immunology/*metabolism/pharmacology
MH  - Carbazoles/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - Extinction, Psychological/drug effects/*physiology
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Indole Alkaloids/pharmacology
MH  - Male
MH  - Prefrontal Cortex/drug effects/*physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, trkB/genetics/metabolism
MH  - Signal Transduction/*physiology
MH  - Taste/*physiology
MH  - Time Factors
PMC - PMC6608190
OTO - NOTNLM
OT  - basolateral amygdala
OT  - brain-derived neurotrophic factor
OT  - conditioned taste aversion
OT  - extinction
OT  - infralimbic prefrontal cortex
EDAT- 2014/05/23 06:00
MHDA- 2014/07/12 06:00
PMCR- 2014/11/21
CRDT- 2014/05/23 06:00
PHST- 2014/05/23 06:00 [entrez]
PHST- 2014/05/23 06:00 [pubmed]
PHST- 2014/07/12 06:00 [medline]
PHST- 2014/11/21 00:00 [pmc-release]
AID - 34/21/7302 [pii]
AID - 5030-13 [pii]
AID - 10.1523/JNEUROSCI.5030-13.2014 [doi]
PST - ppublish
SO  - J Neurosci. 2014 May 21;34(21):7302-13. doi: 10.1523/JNEUROSCI.5030-13.2014.