The metabolism of l-DOPA and l-threo-3,4-dihydroxyphenylserine and their effects on monoamines in the human brain: analysis of the intraventricular fluid from parkinsonian patients

Maruyama, Wakako; Naoi, Makoto; Narabayashi, Hirotaro

doi:10.1016/0022-510x(96)00049-4

Cited by 52 publications

(31 citation statements)

References 11 publications

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“…This hypothesis would concur with current models of striatal dopamine function (Gruber, Dayan, Gutkin, & Solla, 2006;Frank, 2005) and should be tested in a future controlled medication withdrawal study. However, attentional set shifting has previously been shown to be insensitive to dopaminergic medication in PD (Slabosz et al, 2006;Lewis et al, 2005;Cools et al, 2001a;Owen et al, 1993), which acts primarily by restoring striatal dopamine levels (Maruyama, Naoi, & Narabayashi, 1996;Hornykiewicz, 1974). Therefore, we argue that it is more likely that the disproportionate control by bottom-up attention reflects an abnormality that does not involve striatal dopamine.…”

Section: Discussionmentioning

confidence: 76%

Top–Down Attentional Control in Parkinson's Disease: Salient Considerations

Cools

Rogers

Barker³

et al. 2010

Journal of Cognitive Neuroscience

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Abstract■ Cognitive dysfunction in Parkinsonʼs disease (PD) has been hypothesized to reflect a failure of cortical control. In keeping with this hypothesis, some of the cognitive deficits in PD resemble those seen in patients with lesions in the lateral pFC, which has been associated with top-down attentional control. However, there is no direct evidence for a failure of top-down control mechanisms in PD. Here we fill this gap by demonstrating disproportionate control by bottom-up attention to dimensional salience during attentional set shifting. Patients needed significantly more trials to criterion than did controls when shifting to a low-salient dimension while, remarkably, needing significantly fewer trials to criterion than did controls when shifting to a highsalient dimension. Thus, attention was captured by bottom-up attention to salient information to a greater extent in patients than in controls. The results provide a striking reinterpretation of prior set-shifting data and provide the first direct evidence for a failure of top-down attentional control, resembling that seen after catecholamine depletion in the pFC. ■

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Section: Discussionmentioning

confidence: 76%

Top–Down Attentional Control in Parkinson's Disease: Salient Considerations

Cools

Rogers

Barker³

et al. 2010

Journal of Cognitive Neuroscience

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“…The most common treatments for PD are DA agonists and levodopa (L-Dopa), a DA precursor (Maruyama, Naoi, & Narabayashi, 1996). Many cognitive studies in PD do not take into account the level of medication administered to the patient, somewhat confounding the interpretation of experimental results.…”

Section: Deficits Induced By Dopaminergic Medicationmentioning

confidence: 99%

Dynamic Dopamine Modulation in the Basal Ganglia: A Neurocomputational Account of Cognitive Deficits in Medicated and Nonmedicated Parkinsonism

Frank

2005

Journal of Cognitive Neuroscience

847

1,071

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Abstract& Dopamine (DA) depletion in the basal ganglia (BG) of Parkinson's patients gives rise to both frontal-like and implicit learning impairments. Dopaminergic medication alleviates some cognitive deficits but impairs those that depend on intact areas of the BG, apparently due to DA ''overdose.'' These findings are difficult to accommodate with verbal theories of BG/DA function, owing to complexity of system dynamics: DA dynamically modulates function in the BG, which is itself a modulatory system. This article presents a neural network model that instantiates key biological properties and provides insight into the underlying role of DA in the BG during learning and execution of cognitive tasks. Specifically, the BG modulates the execution of ''actions'' (e.g., motor responses and working memory updating) being considered in different parts of the frontal cortex. Phasic changes in DA, which occur during error feedback, dynamically modulate the BG threshold for facilitating/suppressing a cortical command in response to particular stimuli. Reduced dynamic range of DA explains Parkinson and DA overdose deficits with a single underlying dysfunction, despite overall differences in raw DA levels. Simulated Parkinsonism and medication effects provide a theoretical basis for behavioral data in probabilistic classification and reversal tasks. The model also provides novel testable predictions for neuropsychological and pharmacological studies, and motivates further investigation of BG/DA interactions with the prefrontal cortex in working memory. &

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“…As levodopa mainly elevates dopamine levels in the striatum [Hornykiewicz, 1974;Maruyama et al 1996], these differential effects are likely due to opposing effects of levodopa in the dorsal and the ventral striatum, which are connected to different cortical areas via segregated frontostriatal loops [Alexander et al 1986]. …”

Section: Acute Cognitive Effects: Levodopamentioning

confidence: 99%

Acute and chronic cognitive effects of levodopa and dopamine agonists on patients with Parkinson’s disease: a review

Poletti

Bonuccelli

2012

Therapeutic Advances in Psychopharmacology

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Abstract:The spatiotemporal progression of dopamine depletion in Parkinson's disease (PD) provides a special model for assessing dopaminergic effects on neural systems with differential baseline dopamine levels. This study aims at reviewing cognitive effects of dopaminergic stimulation in PD. While considering dopaminergic drugs (levodopa or dopamine agonists), temporal intervals (acute or chronic) and cognitive domains, we found that empirical evidence was almost focused on acute effects of levodopa on executive functions. The paucity of empirical evidence suggests that no meaningful conclusions can be actually drawn and further research is needed in relation to: (1) other cognitive domains; (2) the acute cognitive effects of dopamine agonists, as compared with levodopa; (3) possible differences between cognitive effects of different dopamine agonists; (4) the cognitive effects of chronic dopaminergic therapies. The latter issue is of particular clinical interest considering that many PD patients present a mild cognitive impairment: is this cognitive feature worsened or improved by the prolonged dopaminergic therapy? In addition to the potential risk of inducing dyskinesia and behavioral side effects such as impulse control disorders, also cognitive effects of prolonged dopaminergic treatments should be taken in account by clinicians in order to anticipate or to delay their prescription to PD patients.

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The metabolism of l-DOPA and l-threo-3,4-dihydroxyphenylserine and their effects on monoamines in the human brain: analysis of the intraventricular fluid from parkinsonian patients

Cited by 52 publications

References 11 publications

Top–Down Attentional Control in Parkinson's Disease: Salient Considerations

Top–Down Attentional Control in Parkinson's Disease: Salient Considerations

Dynamic Dopamine Modulation in the Basal Ganglia: A Neurocomputational Account of Cognitive Deficits in Medicated and Nonmedicated Parkinsonism

Acute and chronic cognitive effects of levodopa and dopamine agonists on patients with Parkinson’s disease: a review

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