4.7 Article

The basal ganglia and inhibitory mechanisms in response selection: evidence from subliminal priming of motor responses in Parkinson's disease

期刊

BRAIN
卷 127, 期 -, 页码 330-339

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OXFORD UNIV PRESS
DOI: 10.1093/brain/awh043

关键词

basal ganglia; Parkinson's disease; subliminal priming; inhibition; lateralized readiness potential

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Subliminal response priming was used to investigate inhibitory control processes relevant to response selection impairments in Parkinson's disease. Using a backward masking technique, covert activation of left- or right-hand responses was induced without subjects consciously perceiving the stimuli (right- or left-pointing arrows). The masked priming stimuli were followed by visible arrow stimuli, instructing for a left- or right-hand response, at a delay (interstimulus interval, ISI) of 0 or 100 ms. Motor cortex activation was recorded by means of the electroencephalographic lateralized readiness potential (LRP). Parkinson's disease patients (n = 12) were compared with age-matched controls (n = 12) and young controls (n = 10). In young controls, the ISI = 100 ms task effectively invoked inhibition of the subliminally primed responses, as demonstrated by a reversal of prime-target compatibility effects compared with the ISI = 0 ms task. This reversal implied that there was a so-called negative compatibility effect with faster responses and fewer errors when prime and target arrows pointed in opposite directions than when they required the same response. This negative compatibility effect turned into a positive compatibility effect in Parkinson's disease patients, while age-matched controls produced intermediate values. Together, these results support the view that response selection involves competitive, mutually inhibitory interactions between response alternatives, influenced by basal ganglia-thalamocortical mechanisms. As indicated by the reduced inhibition of partially activated responses, Parkinson's disease and, to a lesser degree, normal ageing affect the efficiency of these inhibitory interactions.

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