Detail of fig4a_pat_day0
Project
Title
In vivo time-lapse image of PSD-95-GFP and dendrites filled with DsRed2 in the AFC of patDp/+ mice at day 0.
Description
NA
Release, Updated
2018-11-14
License
CC BY
Kind
Image data
based on Experiment
File Formats
Data size
102.1 MB
Gene symbols
patDp
Protein names
PSD-95
Protein tags
GFP, DsRed2
Datatype
spine dynamics
Molecular Function (MF)
Biological Process (BP)
-
Cellular Component (CC)
spine synapse
(
GO:0106033
)
postsynaptic density
(
GO:0014069
)
Biological Imaging Method
XYZ Scale
XY: 0.1534 micrometer/pixel, Z: 0.75 micrometer/slice
T scale
2 day for each time interval
Image Acquisition
Experiment type
TimeLapse
Microscope type
ConfocalMicroscope
Acquisition mode
LaserScanningConfocalMicroscopy
Contrast method
Fluorescence
Microscope model
Olympus FV-300
Detector model
-
Objective model
XLPlan N, numerical aperture 1.05, Olympus
Filter set
-
Summary of Methods
See details in Isshiki et al. (2014) Nat Commun, 5: 4742.
Related paper(s)
Masaaki Isshiki, Shinji Tanaka, Toshihiko Kuriu, Katsuhiko Tabuchi, Toru Takumi, Shigeo Okabe (2014) Enhanced synapse remodelling as a common phenotype in mouse models of autism., Nature communications, Volume 5, pp. 4742
Published in 2014 Aug 21 (Electronic publication in Aug. 21, 2014, midnight )
- doi: 10.1038/ncomms5742
-
pmid: 25144834
(Abstract) Developmental deficits in neuronal connectivity are considered to be present in patients with autism spectrum disorders (ASDs). Here we examine this possibility by using in vivo spine imaging in the early postnatal cortex of ASD mouse models. Spines are classified by the presence of either the excitatory postsynaptic marker PSD-95 or the inhibitory postsynaptic marker gephyrin. ASD mouse models show consistent upregulation in the dynamics of PSD-95-positive spines, which may subsequently contribute to stable synaptic connectivity. In contrast, spines receiving inputs from the thalamus, detected by the presence of gephyrin clusters, are larger, highly stable and unaffected in ASD mouse models. Importantly, two distinct mouse models, human 15q11-13 duplication and neuroligin-3 R451C point mutation, show highly similar phenotypes in spine dynamics. This selective impairment in dynamics of PSD-95-positive spines receiving intracortical projections may be a core component of early pathological changes and be a potential target of early intervention.(MeSH Terms)
- Animals
- Autistic Disorder/etiology
- Autistic Disorder/physiopathology[major]
- Biomarkers/analysis
- Biomarkers/metabolism
- Carrier Proteins/genetics
- Carrier Proteins/metabolism
- Cell Adhesion Molecules, Neuronal/genetics
- Dendritic Spines/pathology[major]
- Dendritic Spines/physiology
- Disease Models, Animal
- Disks Large Homolog 4 Protein
- Female
- Green Fluorescent Proteins
- Guanylate Kinases/metabolism
- Male
- Membrane Proteins/genetics
- Membrane Proteins/metabolism
- Mice, Inbred C57BL
- Mice, Inbred ICR
- Mice, Mutant Strains
- Nerve Tissue Proteins/genetics
- Post-Synaptic Density
- Pregnancy
- Synapses/physiology
Contact
Shigeo Okabe
, University of Tokyo
, Department of Cellular Neurobiology, Graduate School of Medicine
Contributors
Masaaki Isshiki, Shinji Tanaka, Toshihiko Kuriu, Katsuhiko Tabuchi, Toru Takumi, Shigeo Okabe
OMERO Dataset
OMERO Project
Source