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Engineered mouse mimics cognitive aspects of schizophrenia

the hyperactive dopamine machinery, the researchers created a genetically altered mouse strain in which dopamine receptors were overexpressed only in the striatum. What's more, they engineered the mouse strain so that they could shut down this overexpression by giving the mice the antibiotic doxycycline.

The researchers found that the engineered animals showed no difference from normal mice in their general cognitive functioning, activity level, sensorimotor functioning, or anxiety.

However, the mice did show the same kinds of specific cognitive deficits seen in human schizophrenics. In tests using mazes, the animals showed deficits in "working memory"--the temporary storage of information required for a task. The animals also showed poorer behavioral flexibility; they were less able than normal mice to reverse their association of a particular odor with a reward.

Biochemical analyses of the animals' brains revealed that the excess dopamine receptor activity in the striatum contributed to abnormal prefrontal cortical function.

Importantly, found the researchers, they could not reverse these cognitive deficits by using the antibiotic to damp down the dopamine machinery. This finding suggests that the effect of the abnormal dopamine machinery was developmental, they said.

"If increased activation of [dopamine] receptors indeed contributes to the cognitive deficits of patients with schizophrenia, our data could explain why antipsychotics do not greatly ameliorate cognitive deficits," wrote the researchers. "The physiological alterations that are responsible for cognitive deficits may be present long before the first psychotic episode, when treatment usually commences. Thus, treatment with typical antipsychotics may be too late to reverse the physiological alterations that are responsible for the cognitive deficits."

The researchers cautioned that "Rodent models of schizophrenia have significant limitations. The neuronal
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Source:Cell Press


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