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A study in mice and rats suggests that an imbalance in chloride ions during a child's development in the womb could be a factor for autism.
Children with autism typically begin showing obvious symptoms, such as trouble making eye contact and slow language development, a year or more after birth. A study in mice and rats now hints that prenatal drug treatment could head off  these problems.
The findings, reported today in Science1, do not suggest that autism spectrum disorders can be prevented in children. But researchers not involved in the study say that they add support to a controversial clinical trial suggesting that some children with autism benefited from taking a common diuretic medication called bumetanide2.
In that trial, a team led by neuroscientist Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille gave 60 children bumetanide or a placebo daily for three months. Children who had less severe forms of autism showed mild improvements in social behaviour after taking the drug, and almost no adverse side effects were observed (see 'Diuretic drug improves symptoms of autism').
But autism researchers greeted the results with caution. Many pointed out that the study did not provide a clear biological mechanism that could explain how the drug improved the symptoms of the disorder.

Improved symptoms

The latest study is an attempt to answer such criticisms by identifying a role for the neurotransmitter GABA. Studies in humans and animals have suggested that GABA, which in healthy people typically inhibits the activity in neurons, is altered in autism and instead activates some brain cells. Ben-Ari’s team hypothesized that the system malfunctions at around the time of birth, when GABA-releasing neurons in the developing brain switch from activating neurons to inhibiting them. A drop in the concentration of chloride ions in neurons makes this switch. Thus, bumetanide, which reduces the levels of chloride in cells, might restore inhibitory GABA function and improve autism symptoms.