1. ¹Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA
2. ²Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA

Correspondence: Dr DA Lewis, Department of Psychiatry, University of Pittsburgh, 3811 O'Hara Street, W1651 Biomedical Science Tower, Pittsburgh, PA 15213, USA. Tel: +1 412 624 3934; Fax: +1 412 624 9910; E-mail: lewisda@upmc.edu

Received 17 May 2007; Revised 4 August 2007; Accepted 6 August 2007; Published online 5 September 2007.

Abstract

The core features of schizophrenia include deficits in cognitive processes mediated by the circuitry of the dorsolateral prefrontal cortex (DLPFC). These deficits are associated with a range of molecular and morphological alterations in the DLPFC, each of which could be a cause, consequence, or compensation in relation to other changes, and thus reflect the neuroplasticity of the brain in response to the underlying disease process. In this review, we consider disturbances in excitatory, inhibitory, and modulatory connections of DLPFC circuitry from the perspective of disease- and development-related neuroplasticity and discuss their implications for the identification of novel therapeutic targets.