l-DOPA and psychosis: Evidence for l-DOPA-induced increases in prefrontal cortex dopamine and in serum corticosterone

Carey, Robert J.; Carrera, Marinete Pinheiro; Dai, Huiliang; Tomaz, Carlos; Huston, Joseph P.

doi:10.1016/0006-3223(94)00378-5

Cited by 33 publications

(15 citation statements)

References 23 publications

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“…Several studies also found that dopaminergic medications enhance working memory (WM) performance (Moustafa, Sherman, & Frank, 2008;Lewis, Slabosz, Robbins, Barker, & Owen, 2005). Overall, these studies suggest that increase of dopamine in PFC enhances prefrontal function (Carey et al, 1995), which, in turn, enhances performance in both attentional and WM processes.…”

Section: Relevant Existing Experimental Studiesmentioning

confidence: 94%

“…Based on experimental findings (Silberstein et al, 2005;Kaasinen et al, 2001;Carey et al, 1995), it is likely that dopaminergic medications increase dopamine levels in PFC. Specifically, we simulate an increase in PFC tonic dopamine levels by increasing the gain value of the sigmoidal activation function, as previously proposed by various computational models (Amos, 2000;Cohen & ServanSchreiber, 1992).…”

Section: Model Architecturementioning

confidence: 99%

“…Another similar paradigm is the "slot machine" task (Shohamy et al, 2009), in which paying attention to one cue of a presented multicue pattern leads to sufficiently good, although not optimal, behavior. The abovementioned models also did not incorporate the findings that dopamine medications increase dopamine levels in PFC, as found in experimental studies (Carey et al, 1995).…”

Section: Existing Computational Models Of Attentional and Motor Learningmentioning

confidence: 99%

“…In addition to basal ganglia dysfunction, several studies showed that mesofrontal dopamine is also affected in PD (Tadaiesky et al, 2008;Prediger et al, 2006;Ashby, Alfonso-Reese, Turken, & Waldron, 1998). Furthermore, some argue that dopaminergic medications (including both the dopamine precursor L-dopa and dopaminergic agonists) increase dopamine levels in prefrontal cortex (PFC; see Silberstein et al, 2005;Kaasinen et al, 2001;Carey, Pinheiro-Carrera, Dai, Tomaz, & Huston, 1995).…”

Section: Introductionmentioning

confidence: 99%

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A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients

Moustafa¹,

Gluck²

2011

Journal of Cognitive Neuroscience

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Abstract■ Most existing models of dopamine and learning in Parkinson disease (PD) focus on simulating the role of basal ganglia dopamine in reinforcement learning. Much data argue, however, for a critical role for prefrontal cortex (PFC) dopamine in stimulus selection in attentional learning. Here, we present a new computational model that simulates performance in multicue category learning, such as the "weather prediction" task. The model addresses how PD and dopamine medications affect stimulus selection processes, which mediate reinforcement learning. In this model, PFC dopamine is key for attentional learning, whereas basal ganglia dopamine, consistent with other models, is key for reinforcement and motor learning. The model assumes that competitive dynamics among PFC neurons is the neural mechanism underlying stimulus selection with limited attentional resources, whereas competitive dynamics among striatal neurons is the neural mechanism underlying action selection. According to our model, PD is associated with decreased phasic and tonic dopamine levels in both PFC and basal ganglia. We assume that dopamine medications increase dopamine levels in both the basal ganglia and PFC, which, in turn, increase tonic dopamine levels but decrease the magnitude of phasic dopamine signaling in these brain structures. Increase of tonic dopamine levels in the simulated PFC enhances attentional shifting performance. The model provides a mechanistic account for several phenomena, including (a) medicated PD patients are more impaired at multicue probabilistic category learning than unmedicated patients and (b) medicated PD patients opt out of reversal when there are alternative and redundant cue dimensions. ■

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Section: Relevant Existing Experimental Studiesmentioning

confidence: 94%

Section: Model Architecturementioning

confidence: 99%

Section: Existing Computational Models Of Attentional and Motor Learningmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients

Moustafa¹,

Gluck²

2011

Journal of Cognitive Neuroscience

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“…In the rat, exogenous l-dopa produces a relatively larger and longer lasting increase in DA levels in the prefrontal cortex than in the striatum (Loeffler et al 1997); the resulting prefrontal cortex DA levels correlate highly with serum l-dopa levels (Carey et al 1995). Interestingly, schizophrenia is associated with an increased conversion of administered l-dopa to DA in the prefrontal cortex (Lindstrom et al 1999).…”

Section: Discussionmentioning

confidence: 99%

A meta-analysis of the response to chronic l-dopa in patients with schizophrenia: therapeutic and heuristic implications

Jaskiw

Popli

2004

Psychopharmacology

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Somatic Delivery of Catecholamines in the Striatum Attenuate Parkinsonian Symptoms and Widen the Therapeutic Window of Oral Sinemet in Rats

Lindner

Plone

Mullins

et al. 1997

Experimental Neurology

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l-DOPA and psychosis: Evidence for l-DOPA-induced increases in prefrontal cortex dopamine and in serum corticosterone

Cited by 33 publications

References 23 publications

A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients

A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients

A meta-analysis of the response to chronic l-dopa in patients with schizophrenia: therapeutic and heuristic implications

Somatic Delivery of Catecholamines in the Striatum Attenuate Parkinsonian Symptoms and Widen the Therapeutic Window of Oral Sinemet in Rats

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