Preventing Schizophrenia-Like Phenomena in a Genetic Mouse Model

Although cellular deficits associated with schizophrenia are thought to begin virtually at conception, the disorder ordinarily begins to manifest itself in conjunction with brain maturation during adolescence. To ascertain whether pharmacological interventions might prevent and reduce these deficits, investigators examined parvalbumin neuron plasticity, network function via medial prefrontal cortex (mPFC) oscillations, and cognition via set shifting and social recognition tasks in a mouse model of schizophrenia.

The LgDel^+/- mouse model involves chromosome-16 deletions mimicking the 22q11 deletion syndrome linked to schizophrenia in humans. As adults, these mice exhibit deficits in prefrontal GABAergic parvalbumin-positive interneuron inhibi…