Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism

The results of genetic studies suggest a possible role for SNAP-25 polymorphism in the development of autism spectrum disorders (ASDs); however, there are no data available on whether changes in SNAP-25 expression also affect animals in rodent models of ASD. The aim of the present study was to explo...

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Bibliographic Details
Published in:Journal of molecular neuroscience 2020-09, Vol.70 (9), p.1313-1320
Main Authors: Lenart, Jacek, Bratek, Ewelina, Lazarewicz, Jerzy W., Zieminska, Elzbieta
Format: Article
Language:English
Subjects:
Adequacy
Animal models
Autism
Biomedical and Life Sciences
Biomedicine
Brain
Cell Biology
Cerebellum
Frontal lobe
Gene polymorphism
Gestation
Hippocampus
Males
mRNA
Neurochemistry
Neurology
Neurosciences
Polymerase chain reaction
Polymorphism
Proteins
Proteomics
SNAP-25 protein
Thalidomide
Valproic acid
Western blotting
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Summary:The results of genetic studies suggest a possible role for SNAP-25 polymorphism in the development of autism spectrum disorders (ASDs); however, there are no data available on whether changes in SNAP-25 expression also affect animals in rodent models of ASD. The aim of the present study was to explore this issue. The studies included 1-month-old rats representing valproic acid (VPA)- and thalidomide (THAL)-induced models of autism. Their mothers received single doses of VPA (800 mg/kg) or THAL (500 mg/kg) per os on the 11th day of gestation. SNAP-25 protein content in the cerebellum, hippocampus, and frontal lobe was determined using Western blotting, while changes of mRNA levels of Snap25 gene were determined using real-time polymerase chain reaction. Compared to controls, SNAP-25 content was decreased by approximately 35% in all brain structures tested, in both males and females, exclusively in the VPA group. In contrast to this, Snap25 expression, studied in males, was increased in the hippocampus and cerebellum in both, VPA- and THAL-treated rats. We discuss the compliance of these results with the hypothesized role of SNAP-25 in the pathophysiology of ASD and the adequacy of the experimental models used.
ISSN:0895-8696
1559-1166
DOI:10.1007/s12031-020-01543-6