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Patrick Guilfoile: Clues about autism

One child in 88 has some form of autism, according to recent estimates from the Centers for Disease Control and Prevention.

The number of children diagnosed with autism is increasing, and consequently there is a desire to understand the biology of the disorder in order to find ways to stem the rising tide of cases.

One way scientists study human maladies is by creating an animal model that can be experimentally manipulated and analyzed in detail.

In a recent report, researchers from France studied mice with a mutation in a specific gene (Fmr1), and rats exposed to a drug (valproate) during pregnancy.

Among other responses, affected baby mice and rats call at abnormal frequency when separated from their mothers, showing a lack of normal social interaction characteristic of autism in humans.

In looking at these two models of autism-like behavior, the researchers were trying to find a common thread.

They specifically focused on a neurotransmitter (GABA) that malfunctions in many individuals with autism.

In autistic individuals, this chemical activates nerve cells in the brain, whereas in other individuals, it inhibits these same nerve cells. The autistic mice and rats showed the same pattern as in autistic humans — this neurotransmitter turned on nerve cells, rather than turning them off.

Surprisingly, this neurotransmitter acts the same way in normal fetal mice and rats as it does in autistic individuals, namely it activates nerve cells.

Researchers discovered that oxytocin, a chemical produced by the mother that stimulates birth of the pups, also flips the switch that allows this neurotransmitter to function normally.

In autistic rats and mice, that switch is not thrown, so the autistic mice continue to have the same pattern of nerve stimulation as they did while they were fetuses.

Normal mice, if given a drug that blocks the action of oxytocin at birth, develop autism-like reactions, confirming the importance of this switch.

Next, the scientists tested a medication normally used to treat heart failure (a type of diuretic or “water pill”) to see if it could reverse some of the autism symptoms. (This drug also has the ability to alter nerve cells in a way similar to the way oxytoxin does.)  

The researchers found that administration of the drug prior to birth did reverse the symptoms in autistic mice and rats.

This work has provided new insight into the biology of autism.

Whether this work in mice and rats will translate to humans is an unanswered question.

For example, this report suggests the need for further research on whether the lack of oxytocin from the mother when babies are delivered by Caesarean section could be an issue.

It also suggests the need for further research on whether the induction of labor using synthetic oxytocin raises concerns.  

In any case, this work shows the value of animal research in opening new avenues to understanding autism.

More information is available in an article by Roman Tyzio and others entitled “Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring.” Science 343: 675-679, February 7, 2014.

PATRICK GUILFOILE has a doctorate in bacteriology and is the associate vice president at Bemidji State University.