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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\u00a0mg\/kg) or THAL (500\u00a0mg\/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 level<jats:strike>s<\/jats:strike> of <jats:italic>Snap25<\/jats:italic> 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, <jats:italic>Snap25<\/jats:italic> 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.<\/jats:p>","DOI":"10.1007\/s12031-020-01543-6","type":"journal-article","created":{"date-parts":[[2020,5,4]],"date-time":"2020-05-04T19:03:26Z","timestamp":1588619006000},"page":"1313-1320","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism"],"prefix":"10.1007","volume":"70","author":[{"given":"Jacek","family":"Lenart","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ewelina","family":"Bratek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerzy W.","family":"Lazarewicz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elzbieta","family":"Zieminska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,5,4]]},"reference":[{"key":"1543_CR1","doi-asserted-by":"publisher","first-page":"1569","DOI":"10.1038\/npp.2015.26","volume":"40","author":"T Aida","year":"2015","unstructured":"Aida T et al (2015) Astroglial glutamate transporter deficiency increases synaptic excitability and leads to pathological repetitive behaviors in mice. 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