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models suggest that loss of inhibitory neuron activity plays a key role in schizophrenia. It is further known that the disease is more common among people harboring a genetic variation that reduces levels of the protein dysbindin in the brain, but how this protein is linked to the clinical features of the disease remains unclear. Gregory Carlson et al. (pp. 17595– 17596) reveal a functional association between dysbindin downregulation and inhibitory neuron impairment in mice. The authors found that dysbindin-mutant mice recapitulated a broad set of phenotypes associated with schizophrenia, including abnormalities in high-frequency brain activity in response to auditory stimuli and reduced levels of the protein parvalbumin (PV), a marker for a type of inhibitory neuron. These changes were further associated with deficits in the inhibitory responses of neurons, as monitored by voltage-sensitive dye imaging of a neuronal circuit in mouse brain tissue slices. Together, the findings suggest a possible mechanistic link between an established genetic liability for schizophrenia and the biochemical underpinnings of the disease, implicating disrupted inhibitory neuron activity involving PV-positive cells as the molecular mechanism involved in schizophrenia, according to the authors. — N.Z. October 25, 2011 u vol. 108 u no. 43 u 17571–17856