Alteration of brain volume in IL-6 overexpressing mice related to autism

► IL-6 overexpressing mice display an increase in the total brain volume. ► The lateral ventricle is also enlarged in the IL-6 overexpressing mice. The brain structures surrounding the lateral ventricle were squeezed and deformed from the normal location. ► A mechanism by which IL-6 may be involved...

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Veröffentlicht in:International journal of developmental neuroscience 2012-11, Vol.30 (7), p.554-559
Hauptverfasser: Wei, Hongen, Mori, Susumu, Hua, Kegang, Li, Xiaohong
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Sprache:eng
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Zusammenfassung:► IL-6 overexpressing mice display an increase in the total brain volume. ► The lateral ventricle is also enlarged in the IL-6 overexpressing mice. The brain structures surrounding the lateral ventricle were squeezed and deformed from the normal location. ► A mechanism by which IL-6 may be involved in the pathogenesis of autism is proposed. Abnormal neuroimmune responses have been reported to be associated with autism and could be appropriate targets for pharmacologic intervention. Our previous studies showed that neuroimmune factor, interleukin (IL)-6, was significantly elevated in the fontal cortex and cerebellum of autistic subjects. The IL-6 overexpressing mice displayed several autism-like features as well as an abnormal dendritic spine morphology and synaptic function. The purpose of this study was to examine the volumetric differences in the brain of IL-6 overexpressing mice and compare with corresponding control mice using magnetic resonance imaging. Here we show that IL-6 overexpressing mice display an increase in the total brain volume. In addition, the lateral ventricle is also enlarged in the IL-6 overexpressing mice. The brain structures surrounding the lateral ventricle were squeezed and deformed from the normal location. These results indicate that IL-6 elevation in the brain could mediate neuroanatomical abnormalities. Taking together with our previous findings, a mechanism by which IL-6 may be involved in the pathogenesis of autism is proposed.
ISSN:0736-5748
1873-474X
DOI:10.1016/j.ijdevneu.2012.08.007