PMID- 28374408
OWN - NLM
STAT- MEDLINE
DCOM- 20180716
LR  - 20180716
IS  - 1699-5848 (Electronic)
IS  - 0213-3911 (Linking)
VI  - 33
IP  - 1
DP  - 2018 Jan
TI  - Morphological alterations in the hippocampus of the Ts65Dn mouse model for Down 
      Syndrome correlate with structural plasticity markers.
PG  - 101-115
LID - 10.14670/HH-11-894 [doi]
AB  - Down syndrome (DS) is the most common chromosomal aneuploidy. Although trisomy on 
      chromosome 21 can display variable phenotypes, there is a common feature among 
      all DS individuals: the presence of intellectual disability. This condition is 
      partially attributed to abnormalities found in the hippocampus of individuals 
      with DS and in the murine model for DS, Ts65Dn. To check if all hippocampal areas 
      were equally affected in 4-5 month adult Ts65Dn mice, we analysed the morphology 
      of dentate gyrus granule cells and cornu ammonis pyramidal neurons using Sholl 
      method on Golgi-Cox impregnated neurons. Structural plasticity has been analysed 
      using immunohistochemistry for plasticity molecules followed by densitometric 
      analysis (Brain Derived Neurotrophic Factor (BDNF), Polysialylated form of the 
      Neural Cell Adhesion Molecule (PSA-NCAM) and the Growth Associated Protein 43 
      (GAP43)). We observed an impairment in the dendritic arborisation of granule 
      cells, but not in the pyramidal neurons in the Ts65Dn mice. When we analysed the 
      expression of molecules related to structural plasticity in trisomic mouse 
      hippocampus, we observed a reduction in the expression of BDNF and PSA-NCAM, and 
      an increment in the expression of GAP43. These alterations were restricted to the 
      regions related to dentate granule cells suggesting an interrelation. Therefore 
      the impairment in dendritic arborisation and molecular plasticity is not a 
      general feature of all Down syndrome principal neurons. Pharmacological 
      manipulations of the levels of plasticity molecules could provide a way to 
      restore granule cell morphology and function.
FAU - Villarroya, Olga
AU  - Villarroya O
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
FAU - Ballestin, Raul
AU  - Ballestin R
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
FAU - Lopez-Hidalgo, Rosa
AU  - Lopez-Hidalgo R
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
FAU - Mulet, Maria
AU  - Mulet M
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
FAU - Blasco-Ibanez, Jose Miguel
AU  - Blasco-Ibanez JM
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
FAU - Crespo, Carlos
AU  - Crespo C
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
FAU - Nacher, Juan
AU  - Nacher J
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
AD  - Fundacion Investigacion Hospital Clinico de Valencia, INCLIVA, Valencia, Spain.
AD  - CIBERSAM: Spanish National Network for Research in Mental Health, Spain.
FAU - Gilabert-Juan, Javier
AU  - Gilabert-Juan J
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain.
AD  - Genetics Department, Universitat de Valencia, CIBERSAM, Spain.
FAU - Varea, Emilio
AU  - Varea E
AD  - Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology 
      Department, Universitat de Valencia, Valencia, Spain. emilio.varea@uv.es.
LA  - eng
PT  - Journal Article
DEP - 20170404
PL  - Spain
TA  - Histol Histopathol
JT  - Histology and histopathology
JID - 8609357
RN  - 0 (Biomarkers)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (GAP-43 Protein)
RN  - 0 (Neural Cell Adhesion Molecule L1)
RN  - 0 (Sialic Acids)
RN  - 0 (polysialyl neural cell adhesion molecule)
SB  - IM
MH  - Age Factors
MH  - Animals
MH  - Biomarkers/metabolism
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - CA1 Region, Hippocampal/metabolism/pathology
MH  - Dendrites/metabolism/pathology
MH  - Disease Models, Animal
MH  - Down Syndrome/genetics/*metabolism/*pathology
MH  - GAP-43 Protein/metabolism
MH  - Genetic Predisposition to Disease
MH  - Golgi Apparatus/metabolism/pathology
MH  - Hippocampus/*metabolism/*pathology
MH  - Male
MH  - Mice, Inbred C3H
MH  - Mice, Inbred C57BL
MH  - Neural Cell Adhesion Molecule L1/metabolism
MH  - *Neuronal Plasticity
MH  - Neurons/*metabolism/*pathology
MH  - Phenotype
MH  - Pyramidal Cells/metabolism/pathology
MH  - Sialic Acids/metabolism
EDAT- 2017/04/05 06:00
MHDA- 2018/07/17 06:00
CRDT- 2017/04/05 06:00
PHST- 2017/04/05 06:00 [pubmed]
PHST- 2018/07/17 06:00 [medline]
PHST- 2017/04/05 06:00 [entrez]
AID - HH-11-894 [pii]
AID - 10.14670/HH-11-894 [doi]
PST - ppublish
SO  - Histol Histopathol. 2018 Jan;33(1):101-115. doi: 10.14670/HH-11-894. Epub 2017 
      Apr 4.