PMID- 22832603
OWN - NLM
STAT- MEDLINE
DCOM- 20130404
LR  - 20211021
IS  - 2158-3188 (Electronic)
IS  - 2158-3188 (Linking)
VI  - 1
IP  - 8
DP  - 2011 Aug 9
TI  - Intravenous injection of neural progenitor cells improved depression-like 
      behavior after cerebral ischemia.
PG  - e29
LID - 10.1038/tp.2011.32 [doi]
AB  - Poststroke depression (PSD) occurs in approximately one-third of stroke survivors 
      and is one of the serious sequelae of stroke. The onset of PSD causes delayed 
      functional recovery by rehabilitation and also increases cognitive impairment. 
      However, appropriate strategies for the therapy against ischemia-induced 
      depression-like behaviors still remain to be developed. Such behaviors have been 
      associated with a reduced level of brain-derived neurotrophic factor (BDNF). In 
      addition, accumulating evidence indicates the ability of stem cells to improve 
      cerebral ischemia-induced brain injuries. However, it remains to be clarified as 
      to the effect of neural progenitor cells (NPCs) on PSD and the association 
      between BDNF level and PSD. Using NPCs, we investigated the effect of intravenous 
      injection of NPCs on PSD. We showed that injection of NPCs improved 
      ischemia-induced depression-like behaviors in the forced-swimming test and 
      sucrose preference test without having any effect on the viable area between 
      vehicle- and NPC-injected ischemic rats. The injection of NPCs prevented the 
      decrease in the level of BDNF in the ipsilateral hemisphere. The levels of 
      phosphorylated CREB, ERK and Akt, which have been implicated in events downstream 
      of BDNF signaling, were also decreased after cerebral ischemia. NPC injection 
      inhibited these decreases in the phosphorylation of CREB and ERK, but not that of 
      Akt. Our findings provide evidence that injection of NPCs may have therapeutic 
      potential for the improvement of depression-like behaviors after cerebral 
      ischemia and that these effects might be associated with restoring BDNF-ERK-CREB 
      signaling.
FAU - Moriyama, Y
AU  - Moriyama Y
AD  - Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy 
      and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo, Japan.
FAU - Takagi, N
AU  - Takagi N
FAU - Tanonaka, K
AU  - Tanonaka K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110809
PL  - United States
TA  - Transl Psychiatry
JT  - Translational psychiatry
JID - 101562664
SB  - IM
MH  - Animals
MH  - Behavior, Animal/*physiology
MH  - Brain Ischemia/*complications/physiopathology/*therapy
MH  - Depression/*etiology/physiopathology/*therapy
MH  - Injections, Intravenous
MH  - Male
MH  - Neural Stem Cells/metabolism/*transplantation
MH  - Rats
MH  - Rats, Transgenic
MH  - Rats, Wistar
MH  - Stroke/complications/pathology/physiopathology/*therapy
PMC - PMC3309503
EDAT- 2011/01/01 00:00
MHDA- 2013/04/05 06:00
PMCR- 2011/08/01
CRDT- 2012/07/27 06:00
PHST- 2012/07/27 06:00 [entrez]
PHST- 2011/01/01 00:00 [pubmed]
PHST- 2013/04/05 06:00 [medline]
PHST- 2011/08/01 00:00 [pmc-release]
AID - tp201132 [pii]
AID - 10.1038/tp.2011.32 [doi]
PST - epublish
SO  - Transl Psychiatry. 2011 Aug 9;1(8):e29. doi: 10.1038/tp.2011.32.