PMID- 24607816
OWN - NLM
STAT- MEDLINE
DCOM- 20141215
LR  - 20140418
IS  - 1873-7064 (Electronic)
IS  - 0028-3908 (Linking)
VI  - 81
DP  - 2014 Jun
TI  - Possible additional antidepressant-like mechanism of sodium butyrate: targeting 
      the hippocampus.
PG  - 292-302
LID - S0028-3908(14)00081-1 [pii]
LID - 10.1016/j.neuropharm.2014.02.017 [doi]
AB  - Chromatin remodeling mediated by histone acetylation might be involved in the 
      pathophysiology and the treatment of depression. Recently, it has been reported 
      that the histone deacetylase (HDAC) inhibitors, such as sodium butyrate (SB), 
      could be a potential therapeutic agent for depression treatment. In the present 
      study, we aimed to clarify the antidepressant mechanism of SB in the hippocampus. 
      The mice were exposed to chronic restraint stress (CRS) for 14 consecutive days 
      (2 h/day) to induce depression-like behaviors. To assess depression-like 
      behaviors, sucrose preference test, light dark test (LD), tail suspension test 
      (TST), and forced swim test (FST) were performed after CRS. We observed that CRS 
      decreased HDAC2 and 5 mRNA and protein levels in the hippocampus. In addition, SB 
      co-treatment decreased the depression-like behaviors that are induced by CRS. SB 
      prevented and normalized the phosphorylation of cAMP response element binding 
      protein (pCREB), acetylation of histone H3 (AceH3), HDAC2, and brain-derived 
      neurotrophic factor (BDNF) expression level that were decreased by CRS in the 
      hippocampus. These results suggest that the decreased HDAC2 and 5 expressions in 
      the hippocampus of CRS may be a type of spontaneous coping response against CRS. 
      However, it seems to be unsuccessful to prevent depression induction since 
      reduction of pCREB, AceH3 and BDNF were accompanied by CRS in the hippocampus. 
      Moreover, the reduced AceH3 level may be associated with the decreased pCREB, 
      which appears to lead to the decreased BDNF.
CI  - Copyright (c) 2014 Elsevier Ltd. All rights reserved.
FAU - Han, Arum
AU  - Han A
AD  - Department of Pharmacology, School of Medicine, CHA University, 222 Yatap-dong, 
      Bundang-gu, Seongnam-si, Gyeonggi-do 463-836, South Korea.
FAU - Sung, Yu-Bin
AU  - Sung YB
AD  - Department of Pharmacology, School of Medicine, CHA University, 222 Yatap-dong, 
      Bundang-gu, Seongnam-si, Gyeonggi-do 463-836, South Korea.
FAU - Chung, Soo-Young
AU  - Chung SY
AD  - Department of Pathology, DIRAMS, 40 Jwadong-gil, Jangan-eup, Gijang-gun, Busan 
      619-953, South Korea.
FAU - Kwon, Min-Soo
AU  - Kwon MS
AD  - Department of Pharmacology, School of Medicine, CHA University, 222 Yatap-dong, 
      Bundang-gu, Seongnam-si, Gyeonggi-do 463-836, South Korea. Electronic address: 
      minsoo100@cha.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140305
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Antidepressive Agents)
RN  - 0 (Sweetening Agents)
RN  - 107-92-6 (Butyric Acid)
RN  - 57-50-1 (Sucrose)
RN  - EC 2.3.1.48 (CREB-Binding Protein)
RN  - EC 3.5.1.98 (Histone Deacetylases)
SB  - IM
MH  - Adaptation, Ocular/drug effects
MH  - Animals
MH  - Antidepressive Agents/*pharmacology/therapeutic use
MH  - Butyric Acid/*pharmacology/therapeutic use
MH  - CREB-Binding Protein/genetics/metabolism
MH  - Depression/drug therapy/etiology/*pathology
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Food Preferences/drug effects
MH  - Gene Expression Regulation/*drug effects/physiology
MH  - Hindlimb Suspension/methods
MH  - Hippocampus/drug effects/*physiology
MH  - Histone Deacetylases/genetics/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Stress, Psychological/complications
MH  - Sucrose/administration & dosage
MH  - Sweetening Agents/administration & dosage
MH  - Swimming/psychology
OTO - NOTNLM
OT  - BDNF
OT  - CREB
OT  - Depression
OT  - Hippocampus
OT  - Histone acetylation
OT  - Sodium butyrate
EDAT- 2014/03/13 06:00
MHDA- 2014/12/17 06:00
CRDT- 2014/03/11 06:00
PHST- 2013/08/30 00:00 [received]
PHST- 2014/02/20 00:00 [revised]
PHST- 2014/02/21 00:00 [accepted]
PHST- 2014/03/11 06:00 [entrez]
PHST- 2014/03/13 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
AID - S0028-3908(14)00081-1 [pii]
AID - 10.1016/j.neuropharm.2014.02.017 [doi]
PST - ppublish
SO  - Neuropharmacology. 2014 Jun;81:292-302. doi: 10.1016/j.neuropharm.2014.02.017. 
      Epub 2014 Mar 5.