Teri J. Reutiman

TL;DR: It is demonstrated that GABAA receptors are reduced in three brain regions that have previously been implicated in the pathogenesis of autism, suggesting widespread GABAergic dysfunction in the brains of subjects with autism.

TL;DR: Impairments in Reelin protein and mRNA and Dab 1 mRNA and elevations in Reln receptor VLDLR mRNA demonstrate impairments in the Reelin signaling system in autism, accounting for some of the brain structural and cognitive deficits observed in the disorder.

TL;DR: In this article, the late second trimester infection (E18) in mice may lead to a different pattern of brain gene expression and structural defects in the developing offspring, leading to significant gene alterations in frontal, hippocampal and cerebellar cortices.

TL;DR: Comparison of levels of GABAB receptor subunits in cerebellum, Brodmann’s area 9, and BA40 of subjects with autism and matched controls found decreases in GABBR1 andGABBR2, which may help explain the presence of seizures that are often comorbid with autism, as well as cognitive difficulties prevalent in autism.

TL;DR: Western blotting data for GABBR1 is verified via qRT-PCR and previous work to measure mRNA and protein levels of 3 GABAA subunits previously associated with autism are extended, providing further evidence of impairment of GABAergic signaling in autism.