Author: Gonzalez-Burgos G1, Cho RY2, Lewis DA3.
Affiliation: 1Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburg, Pennsylvania. 2Department of Psychiatry and Behavioral Sciences, University of Texas Health Science Center at Houston, Houston, Texas. 3Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburg, Pennsylvania. Electronic address: lewisda@upmc.edu.
Conference/Journal: Biol Psychiatry.
Date published: 2015 Mar 17
Other:
Pages: S0006-3223(15)00224-3 , Special Notes: doi: 10.1016/j.biopsych.2015.03.010 , Word Count: 153
Abstract
Cognitive deficits are a core clinical feature of schizophrenia but respond poorly to available medications. Thus, understanding the neural basis of these deficits is crucial for the development of new therapeutic interventions. The types of cognitive processes affected in schizophrenia are thought to depend on the precisely timed transmission of information in cortical regions via synchronous oscillations at gamma band frequency. Here, we review 1) data from clinical studies suggesting that induction of frontal cortex gamma oscillations during tasks that engage cognitive or complex perceptual functions is attenuated in schizophrenia; 2) findings from basic neuroscience studies highlighting the features of parvalbumin-positive interneurons that are critical for gamma oscillation production; and 3) results from recent postmortem human brain studies providing additional molecular bases for parvalbumin-positive interneuron alterations in prefrontal cortical circuitry in schizophrenia.
Copyright © 2015 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
KEYWORDS:
Cognition; GABA; Gamma oscillations; Inhibition; Prefrontal cortex; Working memory
PMID: 25863358