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Schizophrenia Gene's Role May Be Broader, More Potent, than Thought
Date:11/19/2009

ircuitry to respond to an experimental perturbation, to be adaptive. The dysbindin mutation was one of very few gene mutations that had this effect,” he says. “The gene’s unique function suggests to us that impaired adaptive plasticity may have particular relevance to the cause or progression of schizophrenia.”

Schizophrenia generally emerges in people in their late teens or early adulthood. It’s possible, says Davis, that normal developmental changes at this stage of life represent a significant stress to ongoing, stable neural function. If so, he says, the capacity of the nervous system to respond to these normal developmental changes – which in a sense are perturbations – may be impaired in people who become schizophrenic.

The next question the researchers will ask,” he says, “is whether absence of the dysbindin gene causes a blockade of adaptive plasticity in mice and whether other genes linked to schizophrenia cause a similar block of adaptive plasticity.”

The study, led by Dion K. Dickman, PhD, a postdoctoral fellow in the Davis lab, also revealed a more general insight into the mechanisms of adaptive plasticity because they were able to rule out the involvement of numerous genes that were previously considered as candidate players.

“We tested numerous mutations that alter neural function, and most showed perfectly fine adaptive plasticity.” he says, “This suggests that there are distinct roles for genes at the synapse, some support normal neural function while a small subset control adaptive plasticity.”

The phenomenon of adaptive plasticity, a burgeoning area of inquiry in the neurosciences, was first recognized more than a decade ago. Early studies by Davis, a pioneer of the field, showed that when genes functioning in the fruit fly nervous system were mutated, the nervous system would compensate and the animals appeared remar
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