Inhibitory neurons in human cortical circuits: substrate for cognitive dysfunction in schizophrenia

- Parvalbumin (PV) cell alterations contribute to cognitive deficits in schizophrenia.
- PV cells have multiple gene expression disturbances that impair their function.
- These disturbances may arise from either cell-autonomous factors or altered inputs.

Schizophrenia is a disorder of cognitive neurodevelopment. At least some of the core cognitive deficits of the illness appear to be the product of impaired gamma frequency oscillations which depend, in part, on the inhibitory actions of a subpopulation of cortical GABA neurons that express the calcium binding protein parvalbumin (PV). Recent studies have revealed new facets of the development of PV neurons in primate neocortex and of the nature of their molecular alterations in individuals with schizophrenia. Other recent studies in model systems provide insight into how these alterations may arise in the course of cortical circuitry development.