Abstract
Though schizophrenia is a difficult disease to model in an animal because of its complexity, by choosing only one of the disease’s several components to model in a mouse, researchers have been successful in linking certain cognitive disorders associated with schizophrenia to overexpression of the dopamine type 2 receptor. Moreover, they have demonstrated that these cognitive deficits stem from development. Temporarily switching off D2 overexpression has no significant effect on observed deficits, which explains why several drugs targeting the receptor improve behavioral symptoms but have no effect on improving cognitive function.