Sunny J Dutra1,2, Vincent Man3, Hedy Kober4,5, William A Cunningham3, June Gruber6. 1. Boston University School of Medicine, Boston, MA, USA. 2. VA Boston Healthcare System, Boston, MA, USA. 3. Department of Psychology, University of Toronto, Toronto, Canada. 4. Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. 5. Department of Psychology, Yale University, New Haven, CT, USA. 6. Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, CO, USA.
Abstract
OBJECTIVES: Bipolar disorder (BD) is associated with elevated reward sensitivity and persistent positive affect, yet the neural mechanisms underlying these patterns are not well understood. In the present study, we examined putative disruptions in communication within a well-known cortico-limbic reward circuit during reward processing as a potential contributing mechanism to these symptoms. METHODS: The present investigation employed a within- and between-subjects design utilizing a monetary and social incentive delay task among adults with bipolar disorder type I (BD; N = 24) and a healthy non-psychiatric control group (HC; N = 25) during functional magnetic resonance imaging (fMRI). Participants in the BD group were remitted at the time of testing. RESULTS: Functional connectivity analyses revealed increased connectivity between the ventral striatum (VS) seed region and orbitofrontal cortex (OFC) as well as the amygdala during processing of reward receipt in the BD group. After omission of expected rewards, the BD group showed decreased functional connectivity between the VS and a medial frontopolar cortex (mFPC) region associated with consideration of behavioral alternatives. Follow-up analyses within the BD group showed that increased VS-OFC connectivity after reward receipt, and decreased VS-mFPC connected after reward omission, were associated with higher levels of subthreshold mania symptoms. CONCLUSIONS: Results point toward potential mechanisms implicated in elevated reward sensitivity in BD. Enhanced VS-OFC connectivity after reward receipt may be involved in elevated valuation of rewards whereas blunted VS-mFPC connectivity after reward omission may reflect a failure to consider behavioral alternatives to reward pursuit.
OBJECTIVES:Bipolar disorder (BD) is associated with elevated reward sensitivity and persistent positive affect, yet the neural mechanisms underlying these patterns are not well understood. In the present study, we examined putative disruptions in communication within a well-known cortico-limbic reward circuit during reward processing as a potential contributing mechanism to these symptoms. METHODS: The present investigation employed a within- and between-subjects design utilizing a monetary and social incentive delay task among adults with bipolar disorder type I (BD; N = 24) and a healthy non-psychiatric control group (HC; N = 25) during functional magnetic resonance imaging (fMRI). Participants in the BD group were remitted at the time of testing. RESULTS: Functional connectivity analyses revealed increased connectivity between the ventral striatum (VS) seed region and orbitofrontal cortex (OFC) as well as the amygdala during processing of reward receipt in the BD group. After omission of expected rewards, the BD group showed decreased functional connectivity between the VS and a medial frontopolar cortex (mFPC) region associated with consideration of behavioral alternatives. Follow-up analyses within the BD group showed that increased VS-OFC connectivity after reward receipt, and decreased VS-mFPC connected after reward omission, were associated with higher levels of subthreshold mania symptoms. CONCLUSIONS: Results point toward potential mechanisms implicated in elevated reward sensitivity in BD. Enhanced VS-OFC connectivity after reward receipt may be involved in elevated valuation of rewards whereas blunted VS-mFPC connectivity after reward omission may reflect a failure to consider behavioral alternatives to reward pursuit.
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