The nature of working memory gating in Parkinson’s disease: A multi-domain signal detection examination

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Abstract

Distractions are ubiquitous; our brains are inundated with task-irrelevant information. Thus, to remember successfully, one must actively maintain relevant information and prevent distraction from entering working memory. Researchers suggest the basal ganglia-prefrontal pathways are vital to this process by acting as a working memory gate. Using Parkinson’s disease as a model of frontostriatal functioning and with signal detection analyses, the present study aims to better characterize the contribution of frontostriatal pathways of this gating process and to determine how it operates across multiple domains. To achieve this, Parkinson’s disease patients and healthy controls completed verbal and spatial working memory tasks consisting of three conditions: low-load without distraction; low-load with distraction; and high-load without distraction. Patients were tested both ON and OFF dopaminergic medication, allowing for assessment of the contribution of dorsal and ventral frontostriatal pathways. The results demonstrate that when medication is withheld, Parkinson’s patients have a response bias to answer “NO” across all conditions and domains, supporting our hypothesis that the basal ganglia-prefrontal pathways allow or prevent updates of working memory. Contrastingly, medication status affects d′ in the distraction condition but not in the high- or low-load conditions. We attribute this to stimulus valuation processes that were impaired by dopaminergic medication overdosing the ventral pathway. These findings are both consistent with the hypothesis that the working memory gate filters spatial and verbal information before it enters into the working memory system, adding support for the gate being a domain-general mechanism of the central executive.

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Uitvlugt, M. G., Pleskac, T. J., & Ravizza, S. M. (2016). The nature of working memory gating in Parkinson’s disease: A multi-domain signal detection examination. Cognitive, Affective and Behavioral Neuroscience, 16(2), 289–301. https://doi.org/10.3758/s13415-015-0389-9

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