PMID- 23035088
OWN - NLM
STAT- MEDLINE
DCOM- 20130117
LR  - 20231213
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 32
IP  - 40
DP  - 2012 Oct 3
TI  - Extinction of aversive memories associated with morphine withdrawal requires 
      ERK-mediated epigenetic regulation of brain-derived neurotrophic factor 
      transcription in the rat ventromedial prefrontal cortex.
PG  - 13763-75
LID - 10.1523/JNEUROSCI.1991-12.2012 [doi]
AB  - Recent evidence suggests that histone deacetylase (HDAC) inhibitors facilitate 
      extinction of rewarding memory of drug taking. However, little is known about the 
      role of chromatin modification in the extinction of aversive memory of drug 
      withdrawal. In this study, we used conditioned place aversion (CPA), a highly 
      sensitive model for measuring aversive memory of drug withdrawal, to investigate 
      the role of epigenetic regulation of brain-derived neurotrophic factor (BDNF) 
      gene expression in extinction of aversive memory. We found that CPA extinction 
      training induced an increase in recruiting cAMP response element-binding protein 
      (CREB) to and acetylation of histone H3 at the promoters of BDNF exon I 
      transcript and increased BDNF mRNA and protein expression in the ventromedial 
      prefrontal cortex (vmPFC) of acute morphine-dependent rats and that such 
      epigenetic regulation of BDNF gene transcription could be facilitated or 
      diminished by intra-vmPFC infusion of HDAC inhibitor trichostatin A or 
      extracellular signal-regulated kinase (ERK) inhibitor U0126 
      (1,4-diamino-2,3-dicyano-1,4-bis(methylthio)butadiene) before extinction 
      training. Correspondingly, disruption of the epigenetic regulation of BDNF gene 
      transcription with U0126 or suppression of BDNF signaling with Trk receptor 
      antagonist K252a or BDNF scavenger tyrosine kinase receptor B (TrkB)-Fc blocked 
      extinction of CPA behavior. We also found that extinction training-induced 
      activation of ERK and CREB and extinction of CPA behavior could be potentiated or 
      suppressed by intra-vmPFC infusion of d-cycloserine, a NMDA receptor partial 
      agonist or aminophosphonopentanoic acid, a NMDA receptor antagonist. We conclude 
      that extinction of aversive memory of morphine withdrawal requires epigenetic 
      regulation of BDNF gene transcription in the vmPFC through activation of the 
      ERK-CREB signaling pathway perhaps in a NMDA receptor-dependent manner.
FAU - Wang, Wei-Sheng
AU  - Wang WS
AD  - State Key Laboratory of Drug Research, Shanghai Institute of Materia Media, 
      Chinese Academy of Sciences, Shanghai 201203, China.
FAU - Kang, Shuo
AU  - Kang S
FAU - Liu, Wen-Tao
AU  - Liu WT
FAU - Li, Mu
AU  - Li M
FAU - Liu, Yao
AU  - Liu Y
FAU - Yu, Chuan
AU  - Yu C
FAU - Chen, Jie
AU  - Chen J
FAU - Chi, Zhi-Qiang
AU  - Chi ZQ
FAU - He, Ling
AU  - He L
FAU - Liu, Jing-Gen
AU  - Liu JG
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 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Butadienes)
RN  - 0 (Creb1 protein, rat)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Histone Deacetylase Inhibitors)
RN  - 0 (Histones)
RN  - 0 (Nitriles)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (U 0126)
RN  - 76I7G6D29C (Morphine)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Acetylation/drug effects
MH  - Animals
MH  - Association Learning/drug effects/*physiology
MH  - Avoidance Learning/*physiology
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/*genetics
MH  - Butadienes/pharmacology
MH  - Chromatin Assembly and Disassembly/drug effects/physiology
MH  - Conditioning, Classical/drug effects/physiology
MH  - Cyclic AMP Response Element-Binding Protein/physiology
MH  - Epigenetic Repression/drug effects/*physiology
MH  - Extinction, Psychological/*physiology
MH  - Histone Deacetylase Inhibitors/pharmacology
MH  - Histones/physiology
MH  - MAP Kinase Signaling System/drug effects/*physiology
MH  - Male
MH  - Morphine/*toxicity
MH  - Morphine Dependence/*physiopathology
MH  - Nitriles/pharmacology
MH  - Prefrontal Cortex/*physiology
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Protein Processing, Post-Translational/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/antagonists & inhibitors
MH  - Receptors, N-Methyl-D-Aspartate/physiology
MH  - Reward
MH  - Substance Withdrawal Syndrome/*physiopathology
MH  - Transcription, Genetic
PMC - PMC6704794
EDAT- 2012/10/05 06:00
MHDA- 2013/01/18 06:00
PMCR- 2013/04/03
CRDT- 2012/10/05 06:00
PHST- 2012/10/05 06:00 [entrez]
PHST- 2012/10/05 06:00 [pubmed]
PHST- 2013/01/18 06:00 [medline]
PHST- 2013/04/03 00:00 [pmc-release]
AID - 32/40/13763 [pii]
AID - 3801826 [pii]
AID - 10.1523/JNEUROSCI.1991-12.2012 [doi]
PST - ppublish
SO  - J Neurosci. 2012 Oct 3;32(40):13763-75. doi: 10.1523/JNEUROSCI.1991-12.2012.