system development and physiology, from simple trophic support of neurons to wrapping axons to allow for rapid nerve impulse conduction to modulating synaptic connectivity and efficacy. Astrocytes are the most abundant cell type in the brain and they are intimately associated with synapses and govern key steps in synapse formation and plasticity. Recently, a number of studies havesuggested that an abnormal function of glia/astrocytes may play a role in the development of autism.
Objectives: The aim of this study is to determine whether the density and morphology of astrocytes are altered in the brain of autistic subjects.
Methods: Frozen human brain tissues of six autistic subjects (mean age 8.3 ± 3.8 years) and six age-matched normal subjects (mean age 8 ± 3.7 years) were obtained from the NICHD Brain and Tissue Bank for Developmental Disorders. Donors with autism fit the diagnostic criteria of the Diagnostic and Statistical Manual-IV, as confirmed by the Autism Diagnostic Interview-Revised. In this study, Western Blot Analyses, Immunohistochemistry and confocal microscopy studies were used to detect the density and morphology of astrocytes.
Results: In immunohistochemistry studies using anti-GFAP (glial fibrillary acidic protein) antibody, we observed under confocal microscopy that the density of astrocytes were significantly increased in the frontal cortex of autistic subjects as compared with age-matched controls. In addition, we observed that the astrocytes in autistic cortex had significantly decreased branching as compared with controls. However, with western blot analyses, we did not detect significant differences in the protein expression of GFAP in frontal cortex between autistic subjects and the controls.
Conclusions: Our findings suggest that astrocytes are altered in the frontal cortex of autistic subjects and this alteration could affect the function of the astrocytes and consequently the neural synapses formation and plasticity, which may contribute to the pathogenesis of autism.