TY - JOUR
T1 - Cognition and control in schizophrenia
T2 - A computational model of dopamine and prefrontal function
AU - Braver, Todd S.
AU - Barch, Deanna M.
AU - Cohen, Jonathan D.
N1 - Funding Information:
This work was supported by an NIMH ROI (MH47073), Center Grant (MH45156), and NIMH Program Project (MH47566).
Funding Information:
This work was presented at the conference, “Schizophrenia: From Molecule to Public Policy” held in Santa Fe, New Mexico in October 1998. The conference was sponsored by the Society of Biological Psychiatry through an unrestriced educational grant provided by Eli Lilly and Company.
PY - 1999/8/1
Y1 - 1999/8/1
N2 - Behavioral deficits suffered by patients with schizophrenia in a wide array of cognitive domains can be conceptualized as failures of cognitive control, due to an impaired ability to internally represent, maintain, and update context information. A theory is described that postulates a single neurobiological mechanism for these disturbances, involving dysfunctional interactions between the dopamine neurotransmitter system and the prefrontal cortex. Specifically, it is hypothesized that in schizophrenia, there is increased noise in the activity of the dopamine system, leading to abnormal 'gating' of information into prefrontal cortex. The theory is implemented as an explicit connectionist computational model that incorporates the roles of both dopamine and prefrontal cortex in cognitive control. A simulation is presented of behavioral performance in a version of the Continuous Performance Test specifically adapted to measure critical aspects of cognitive control function. Schizophrenia patients exhibit clear behavioral deficits on this task that reflect impairments in both the maintenance and updating of context information. The simulation results suggest that the model can successfully account for these impairments in terms of abnormal dopamine activity. This theory provides a potential point of contact between research on the neurobiological and psychological aspects of schizophrenia, by illustrating how a particular physiological disturbance might lead to precise and quantifiable consequences for behavior. Copyright (C) 1999 Society of Biological Psychiatry.
AB - Behavioral deficits suffered by patients with schizophrenia in a wide array of cognitive domains can be conceptualized as failures of cognitive control, due to an impaired ability to internally represent, maintain, and update context information. A theory is described that postulates a single neurobiological mechanism for these disturbances, involving dysfunctional interactions between the dopamine neurotransmitter system and the prefrontal cortex. Specifically, it is hypothesized that in schizophrenia, there is increased noise in the activity of the dopamine system, leading to abnormal 'gating' of information into prefrontal cortex. The theory is implemented as an explicit connectionist computational model that incorporates the roles of both dopamine and prefrontal cortex in cognitive control. A simulation is presented of behavioral performance in a version of the Continuous Performance Test specifically adapted to measure critical aspects of cognitive control function. Schizophrenia patients exhibit clear behavioral deficits on this task that reflect impairments in both the maintenance and updating of context information. The simulation results suggest that the model can successfully account for these impairments in terms of abnormal dopamine activity. This theory provides a potential point of contact between research on the neurobiological and psychological aspects of schizophrenia, by illustrating how a particular physiological disturbance might lead to precise and quantifiable consequences for behavior. Copyright (C) 1999 Society of Biological Psychiatry.
KW - Computational model
KW - Inhibition
KW - Neural network
KW - Neuromodulation
KW - Reinforcement learning
KW - Working memory
UR - http://www.scopus.com/inward/record.url?scp=0032765150&partnerID=8YFLogxK
U2 - 10.1016/S0006-3223(99)00116-X
DO - 10.1016/S0006-3223(99)00116-X
M3 - Article
C2 - 10435197
AN - SCOPUS:0032765150
SN - 0006-3223
VL - 46
SP - 312
EP - 328
JO - Biological Psychiatry
JF - Biological Psychiatry
IS - 3
ER -