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Comment on "Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring"
Victorio Bambini-Junior1, Gustavo Della Flora Nunes2, Tomasz Schneider3
1Federal University of Rio Grande do Sul, Research Group in Neuroglial Plasticity at the Department of Biochemistry, Institute of Health's Basic Science, Porto Alegre, Rio Grande do Sul, Brazil. Federal University of Rio Grande do Sul, Translational Research Group in Autism Spectrum Disorders (GETTEA), Porto Alegre, RS, Brazil. victoriobambini@gmail.com.
Tyzio et al. (Reports, 7 February 2014, p. 675) reported that bumetanide restored the impaired oxytocin-mediated γ-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery in animal models of autism, ameliorating some autistic-like characteristics in the offspring. However, standard practices in the study of these models, such as the use of sex-dimorphic or males-only analyses and implementation of tests measuring social behavior, are lacking to definitely associate their findings to autism.
Tyzio et al. (Reports, 7 February 2014, p. 675) reported that bumetanide restored the impaired oxytocin-mediated γ-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery in animal models of autism, ameliorating some autistic-like characteristics in the offspring. However, standard practices in the study of these models, such as the use of sex-dimorphic or males-only analyses and implementation of tests measuring social behavior, are lacking to definitely associate their findings to autism.
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