PMID- 24904293
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140606
LR  - 20220309
IS  - 1662-5102 (Print)
IS  - 1662-5102 (Electronic)
IS  - 1662-5102 (Linking)
VI  - 8
DP  - 2014
TI  - Distinctive behavioral and cellular responses to fluoxetine in the mouse model 
      for Fragile X syndrome.
PG  - 150
LID - 10.3389/fncel.2014.00150 [doi]
LID - 150
AB  - Fluoxetine is used as a therapeutic agent for autism spectrum disorder (ASD), 
      including Fragile X syndrome (FXS). The treatment often associates with 
      disruptive behaviors such as agitation and disinhibited behaviors in FXS. To 
      identify mechanisms that increase the risk to poor treatment outcome, we 
      investigated the behavioral and cellular effects of fluoxetine on adult Fmr1 
      knockout (KO) mice, a mouse model for FXS. We found that fluoxetine reduced 
      anxiety-like behavior of both wild-type and Fmr1 KO mice seen as shortened 
      latency to enter the center area in the open field test. In Fmr1 KO mice, 
      fluoxetine normalized locomotor hyperactivity but abnormally increased 
      exploratory activity. Reduced brain-derived neurotrophic factor (BDNF) and 
      increased TrkB receptor expression levels in the hippocampus of Fmr1 KO mice 
      associated with inappropriate coping responses under stressful condition and 
      abolished antidepressant activity of fluoxetine. Fluoxetine response in the cell 
      proliferation was also missing in the hippocampus of Fmr1 KO mice when compared 
      with wild-type controls. The postnatal mRNA expression of serotonin transporter 
      (SERT) was reduced in the thalamic nuclei of Fmr1 KO mice during the time of 
      transient innervation of somatosensory neurons suggesting that developmental 
      changes of SERT expression were involved in the differential cellular and 
      behavioral responses to fluoxetine in wild-type and Fmr1 mice. The results 
      indicate that changes of BDNF/TrkB signaling contribute to differential 
      behavioral responses to fluoxetine among individuals with ASD.
FAU - Uutela, Marko
AU  - Uutela M
AD  - Institute of Biomedicine/Physiology, University of Helsinki Helsinki, Finland.
FAU - Lindholm, Jesse
AU  - Lindholm J
AD  - Neuroscience Center, University of Helsinki Helsinki, Finland.
FAU - Rantamaki, Tomi
AU  - Rantamaki T
AD  - Neuroscience Center, University of Helsinki Helsinki, Finland.
FAU - Umemori, Juzoh
AU  - Umemori J
AD  - Neuroscience Center, University of Helsinki Helsinki, Finland.
FAU - Hunter, Kerri
AU  - Hunter K
AD  - Institute of Biomedicine/Physiology, University of Helsinki Helsinki, Finland.
FAU - Voikar, Vootele
AU  - Voikar V
AD  - Neuroscience Center, University of Helsinki Helsinki, Finland.
FAU - Castren, Maija L
AU  - Castren ML
AD  - Institute of Biomedicine/Physiology, University of Helsinki Helsinki, Finland ; 
      Department of Child Neurology, Hospital for Children and Adolescents, University 
      Hospital of Helsinki Helsinki, Finland.
LA  - eng
PT  - Journal Article
DEP - 20140528
PL  - Switzerland
TA  - Front Cell Neurosci
JT  - Frontiers in cellular neuroscience
JID - 101477935
PMC - PMC4036306
OTO - NOTNLM
OT  - BDNF
OT  - TrkB receptors
OT  - autism
OT  - behavior
OT  - neurogenesis
EDAT- 2014/06/07 06:00
MHDA- 2014/06/07 06:01
PMCR- 2014/01/01
CRDT- 2014/06/07 06:00
PHST- 2014/01/17 00:00 [received]
PHST- 2014/05/09 00:00 [accepted]
PHST- 2014/06/07 06:00 [entrez]
PHST- 2014/06/07 06:00 [pubmed]
PHST- 2014/06/07 06:01 [medline]
PHST- 2014/01/01 00:00 [pmc-release]
AID - 10.3389/fncel.2014.00150 [doi]
PST - epublish
SO  - Front Cell Neurosci. 2014 May 28;8:150. doi: 10.3389/fncel.2014.00150. 
      eCollection 2014.