Expression of SHANK3 in the Temporal Neocortex of Patients with Intractable Temporal Epilepsy and Epilepsy Rat Models

SH3 and multiple ankyrin (ANK) repeat domain 3 (SHANK3) is a synaptic scaffolding protein enriched in the postsynaptic density of excitatory synapses. SHANK3 plays an important role in the formation and maturation of excitatory synapses. In the brain, SHANK3 directly or indirectly interacts with var...

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Published in:Cellular and molecular neurobiology 2017-07, Vol.37 (5), p.857-867
Main Authors: Zhang, Yanke, Gao, Baobing, Xiong, Yan, Zheng, Fangshuo, Xu, Xin, Yang, Yong, Hu, Yida, Wang, Xuefeng
Format: Article
Language:English
Subjects:
Adult
Animal models
Animals
Ankyrins
Autism
Behavior, Animal
Biomedical and Life Sciences
Biomedicine
Case-Control Studies
Cell Biology
Demography
Disease Models, Animal
Epilepsy
Epilepsy, Temporal Lobe - metabolism
Epilepsy, Temporal Lobe - pathology
Female
Glutamic acid receptors (metabotropic)
Hippocampus - metabolism
Hippocampus - pathology
Humans
Immunofluorescence
Immunohistochemistry
Isoforms
Male
N-Methyl-D-aspartic acid receptors
Neocortex - metabolism
Neocortex - pathology
Nerve Tissue Proteins - metabolism
Neurobiology
Neurosciences
Original Research
Pilocarpine
Postsynaptic density
Rats, Sprague-Dawley
Rodents
Seizures
Synaptic plasticity
Synaptic transmission
Temporal cortex
Temporal lobe
Temporal Lobe - metabolism
Temporal Lobe - pathology
Young Adult
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Summary:SH3 and multiple ankyrin (ANK) repeat domain 3 (SHANK3) is a synaptic scaffolding protein enriched in the postsynaptic density of excitatory synapses. SHANK3 plays an important role in the formation and maturation of excitatory synapses. In the brain, SHANK3 directly or indirectly interacts with various synaptic molecules including N-methyl-D-aspartate receptor, the metabotropic glutamate receptor (mGluR), and α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Previous studies have shown that Autism spectrum disorder is a result of mutations of the main SHANK3 isoforms, which may be due to deficit in excitatory synaptic transmission and plasticity. Recently, accumulating evidence has demonstrated that overexpression of SHANK3 could induce seizures in vivo. However, little is known about the role of SHANK3 in refractory temporal lobe epilepsy (TLE). Therefore, we investigated the expression pattern of SHANK3 in patients with intractable temporal lobe epilepsy and in pilocarpine-induced models of epilepsy. Immunofluorescence, immunohistochemistry, and western blot analysis were used to locate and determine the expression of SHANK3 in the temporal neocortex of patients with epilepsy, and in the hippocampus and temporal lobe cortex of rats in a pilocarpine-induced epilepsy model. Double-labeled immunofluorescence showed that SHANK3 was mainly expressed in neurons. Western blot analysis confirmed that SHANK3 expression was increased in the neocortex of TLE patients and rats. These results indicate that SHANK3 participates in the pathology of epilepsy.
ISSN:0272-4340
1573-6830
DOI:10.1007/s10571-016-0423-7