PMID- 24369067
OWN - NLM
STAT- MEDLINE
DCOM- 20140801
LR  - 20211021
IS  - 1750-1326 (Electronic)
IS  - 1750-1326 (Linking)
VI  - 8
DP  - 2013 Dec 26
TI  - Behavioral and transcriptome alterations in male and female mice with postnatal 
      deletion of TrkB in dorsal striatal medium spiny neurons.
PG  - 47
LID - 10.1186/1750-1326-8-47 [doi]
AB  - BACKGROUND: The high affinity tyrosine kinase receptor, TrkB, is the primary 
      receptor for brain derived neurotrophic factor (BDNF) and plays an important role 
      in development, maintenance and plasticity of the striatal output medium size 
      spiny neuron. The striatal BDNF/TrkB system is thereby implicated in many 
      physiologic and pathophysiologic processes, the latter including mood disorders, 
      addiction, and Huntington's disease. We crossed a mouse harboring a transgene 
      directing cre-recombinase expression primarily to postnatal, dorsal striatal 
      medium spiny neurons, to a mouse containing a floxed TrkB allele (fB) mouse 
      designed for deletion of TrkB to determine its role in the adult striatum. 
      RESULTS: We found that there were sexually dimorphic alterations in behaviors in 
      response to stressful situations and drugs of abuse. Significant sex and/or 
      genotype differences were found in the forced swim test of depression-like 
      behaviors, anxiety-like behaviors on the elevated plus maze, and cocaine 
      conditioned reward. Microarray analysis of dorsal striatum revealed significant 
      dysregulation in individual and groups of genes that may contribute to the 
      observed behavioral responses and in some cases, represent previously 
      unidentified downstream targets of TrkB. CONCLUSIONS: The data point to a set of 
      behaviors and changes in gene expression following postnatal deletion of TrkB in 
      the dorsal striatum distinct from those in other brain regions.
FAU - Unterwald, Ellen M
AU  - Unterwald EM
FAU - Page, Michelle E
AU  - Page ME
FAU - Brown, Timothy B
AU  - Brown TB
FAU - Miller, Jonathan S
AU  - Miller JS
FAU - Ruiz, Marta
AU  - Ruiz M
FAU - Pescatore, Karen A
AU  - Pescatore KA
FAU - Xu, Baoji
AU  - Xu B
FAU - Reichardt, Louis French
AU  - Reichardt LF
FAU - Beverley, Joel
AU  - Beverley J
FAU - Tang, Bin
AU  - Tang B
FAU - Steiner, Heinz
AU  - Steiner H
FAU - Thomas, Elizabeth A
AU  - Thomas EA
FAU - Ehrlich, Michelle E
AU  - Ehrlich ME
AD  - Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA 
      19107, USA. michelle.ehrlich@mssm.edu.
LA  - eng
GR  - R01 NS081485/NS/NINDS NIH HHS/United States
GR  - DA011261/DA/NIDA NIH HHS/United States
GR  - T32 DA007237/DA/NIDA NIH HHS/United States
GR  - DA022422/DA/NIDA NIH HHS/United States
GR  - P30 DA013429/DA/NIDA NIH HHS/United States
GR  - R01 NS050596/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20131226
PL  - England
TA  - Mol Neurodegener
JT  - Molecular neurodegeneration
JID - 101266600
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Behavior, Animal/*physiology
MH  - Blotting, Western
MH  - Corpus Striatum/*metabolism
MH  - Female
MH  - Gene Knockdown Techniques
MH  - In Situ Hybridization
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Neurons/*metabolism
MH  - Oligonucleotide Array Sequence Analysis
MH  - Receptor, trkB/*deficiency/*genetics
MH  - Signal Transduction/genetics
MH  - Transcriptome
PMC - PMC3880973
EDAT- 2013/12/27 06:00
MHDA- 2014/08/02 06:00
PMCR- 2013/12/26
CRDT- 2013/12/27 06:00
PHST- 2013/11/28 00:00 [received]
PHST- 2013/12/19 00:00 [accepted]
PHST- 2013/12/27 06:00 [entrez]
PHST- 2013/12/27 06:00 [pubmed]
PHST- 2014/08/02 06:00 [medline]
PHST- 2013/12/26 00:00 [pmc-release]
AID - #N/A [pii]
AID - 1750-1326-8-47 [pii]
AID - 10.1186/1750-1326-8-47 [doi]
PST - epublish
SO  - Mol Neurodegener. 2013 Dec 26;8:47. doi: 10.1186/1750-1326-8-47.