Early continuous inhibition of group 1 mGlu signaling partially rescues dendritic spine abnormalities in the Fmr1 knockout mouse model for fragile X syndrome

2010 ◽  
Vol 215 (2) ◽  
pp. 291-300 ◽  
Author(s):  
Tao Su ◽  
Hong-Xing Fan ◽  
Tao Jiang ◽  
Wei-Wen Sun ◽  
Wei-Yi Den ◽  
...  
Keyword(s):  
Mouse Model ◽  
Fragile X Syndrome ◽  
Dendritic Spine ◽  
Knockout Mouse ◽  
Fragile X ◽  
Knockout Mouse Model ◽  
Spine Abnormalities ◽  
Fmr1 Knockout Mouse ◽  
Group 1

scholarly journals Altered anxiety-related and social behaviors in the Fmr1 knockout mouse model of fragile X syndrome

2005 ◽  
Vol 4 (7) ◽  
pp. 420-430 ◽  
Author(s):  
C. M. Spencer ◽  
O. Alekseyenko ◽  
E. Serysheva ◽  
L. A. Yuva-Paylor ◽  
R. Paylor
Keyword(s):  
Mouse Model ◽  
Fragile X Syndrome ◽  
Knockout Mouse ◽  
Fragile X ◽  
Social Behaviors ◽  
Knockout Mouse Model ◽  
Fmr1 Knockout Mouse

scholarly journals Multifaceted Changes in Synaptic Composition and Astrocytic Involvement in a Mouse Model of Fragile X Syndrome

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Anish K. Simhal ◽  
Yi Zuo ◽  
Marc M. Perez ◽  
Daniel V. Madison ◽  
Guillermo Sapiro ◽  
...  
Keyword(s):  
Mouse Model ◽  
Fragile X Syndrome ◽  
Knockout Mouse ◽  
Fragile X ◽  
Inhibitory Synapses ◽  
Excitatory Synapses ◽  
Array Tomography ◽  
Layer 4 ◽  
Fmr1 Knockout Mouse ◽  
Circuit Function

Abstract Fragile X Syndrome (FXS), a common inheritable form of intellectual disability, is known to alter neocortical circuits. However, its impact on the diverse synapse types comprising these circuits, or on the involvement of astrocytes, is not well known. We used immunofluorescent array tomography to quantify different synaptic populations and their association with astrocytes in layers 1 through 4 of the adult somatosensory cortex of a FXS mouse model, the FMR1 knockout mouse. The collected multi-channel data contained approximately 1.6 million synapses which were analyzed using a probabilistic synapse detector. Our study reveals complex, synapse-type and layer specific changes in the neocortical circuitry of FMR1 knockout mice. We report an increase of small glutamatergic VGluT1 synapses in layer 4 accompanied by a decrease in large VGluT1 synapses in layers 1 and 4. VGluT2 synapses show a rather consistent decrease in density in layers 1 and 2/3. In all layers, we observe the loss of large inhibitory synapses. Lastly, astrocytic association of excitatory synapses decreases. The ability to dissect the circuit deficits by synapse type and astrocytic involvement will be crucial for understanding how these changes affect circuit function, and ultimately defining targets for therapeutic intervention.

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