PMID- 18544182
OWN - NLM
STAT- MEDLINE
DCOM- 20090313
LR  - 20161020
IS  - 1461-1457 (Print)
IS  - 1461-1457 (Linking)
VI  - 12
IP  - 1
DP  - 2009 Feb
TI  - Single immobilization stress differentially alters the expression profile of 
      transcripts of the brain-derived neurotrophic factor (BDNF) gene and histone 
      acetylation at its promoters in the rat hippocampus.
PG  - 73-82
LID - 10.1017/S1461145708008997 [doi]
AB  - Decreased levels of brain-derived neurotrophic factor (BDNF) in the hippocampus 
      are implicated in the pathophysiology of major depression, although the mechanism 
      has yet to be characterized. Epigenetic studies revealed that DNA methylation and 
      histone modifications at the promoter of exons of the BDNF gene are the pivotal 
      factors in the regulation of BDNF transcription. Histone acetylation regulates 
      gene transcription through chromatin remodelling. We examined the influence of a 
      single immobilization stress (SIS) at 2 h and 24 h afterwards on the levels of 
      total BDNF mRNA with each exon mRNA by quantitative real-time PCR, acetylated 
      histone at the promoters of the BDNF gene by chromatin immunoprecipitation 
      followed by real-time PCR, and BDNF protein by ELISA in the rat hippocampus. SIS 
      significantly decreased the levels of total BDNF mRNA with significantly reduced 
      levels of exons I and IV mRNA followed by a significant reduction in BDNF protein 
      4 h after SIS. Significant decreases in the levels of acetylated histone H3, but 
      not H4, were found at the promoters of exons I, IV, and VI. In contrast, no 
      marked changes in the levels of either acetylated histone or BDNF mRNA and 
      protein were found 24 h after SIS. This study demonstrated the involvement of 
      histone acetylation in the regulation of BDNF transcription by SIS, and the 
      plastic change in histone acetylation after SIS. These findings suggest that 
      stress affects BDNF gene transcription via epigenetic regulation, and 
      glucocorticoid may be involved in this regulation.
FAU - Fuchikami, Manabu
AU  - Fuchikami M
AD  - Department of Psychiatry and Neurosciences, Division of Frontier Medicine, 
      Graduate School of Medical Sciences, Hiroshima University, Hiroshima, Japan.
FAU - Morinobu, Shigeru
AU  - Morinobu S
FAU - Kurata, Akiko
AU  - Kurata A
FAU - Yamamoto, Shigeto
AU  - Yamamoto S
FAU - Yamawaki, Shigeto
AU  - Yamawaki S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080611
PL  - England
TA  - Int J Neuropsychopharmacol
JT  - The international journal of neuropsychopharmacology
JID - 9815893
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Histones)
RN  - 0 (Untranslated Regions)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Acetylation
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis/genetics
MH  - Chromatin Immunoprecipitation
MH  - Corticosterone/blood
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Exons/genetics
MH  - Hippocampus/*metabolism
MH  - Histones/*metabolism
MH  - Male
MH  - Promoter Regions, Genetic/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Restraint, Physical
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Stress, Psychological/metabolism/*psychology
MH  - Untranslated Regions/genetics
EDAT- 2008/06/12 09:00
MHDA- 2009/03/14 09:00
CRDT- 2008/06/12 09:00
PHST- 2008/06/12 09:00 [pubmed]
PHST- 2009/03/14 09:00 [medline]
PHST- 2008/06/12 09:00 [entrez]
AID - S1461145708008997 [pii]
AID - 10.1017/S1461145708008997 [doi]
PST - ppublish
SO  - Int J Neuropsychopharmacol. 2009 Feb;12(1):73-82. doi: 10.1017/S1461145708008997. 
      Epub 2008 Jun 11.