redOrbit Staff & Wire Reports Your Universe Online
A drug given to pregnant mice with models of autism prevents autistic behavior in their offspring, according to a new study reported Friday in the journal Science.
Although the drug could not be administered prenatally in humans since there is no way to screen for autism in human fetuses, clinical trials in which the drug was administered to young children who have already developed autistic symptoms are showing progress, the researchers said.
The causes of autism spectrum disorder, or ASD, are complex and not well understood, although experts generally agree that the disorder has its origins in early life fetal and/or postnatal.
Neurons contain high levels of chloride throughout the entire embryonic phase. As a result, GABA, the main chemical messenger of the brain, excites the neurons instead of inhibiting them in order to facilitate brain construction. Subsequently, a natural reduction in chloride levels allows GABA to exercise its inhibitory role and regulate the activity of the adolescent/adult brain.
In the current study, researchers made a breakthrough in understanding ASD by demonstrating that chloride levels are not only elevated in the neurons of mice used in an animal model of autism, but they remain at abnormal levels from birth.
These results corroborate the success obtained with the diuretic treatment (which reduces neuronal chloride levels) tested on autistic children in 2012, and suggest that administration of diuretics to pregnant mice before birth corrects the deficits in the offspring. The study also showed that the birth hormone oxytocin brings about a decrease in chloride level during birth, which controls the expression of the autistic syndrome.
In the current study, the researchers used two rodent models of ASD one caused by a gene and one caused by the environmental factor of exposure to the drug valproate in utero.
Oxytocin didnt signal from mother to baby in either model, and as a result, chloride built to higher concentrations than it should have inside fetal neurons. However, by injecting the mothers with bumetanide, the researchers were able to reduce chloride levels to their appropriate amount and in turn restore the GABA switch mechanism from excitatory to inhibitory, as expected.
Critically, offspring exposed to this treatment, which was administered one day before delivery, didnt demonstrate traits of autism.
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Using Bumetanide For Chloride Reduction May Prevent Autism