Two experiments examined the issue of the functional mechanisms exerting a modulatory effect on the latency of the P3. In experiment 1, using a psychological refractory period (PRP) paradigm, two sequential stimuli (T1 and T2) were presented in each trial at varying stimulus onset asynchronies (SOAs), each requiring a speeded choice response. Substantial lengthening of the reaction time to T2 was observed as SOA decreased (i.e., PRP effect). A systematic investigation of the T2-locked P3 component amplitude and latency was undertaken to discover whether either of these P3 parameters was correlated with the PRP effect. The results showed lengthening of the T2-locked P3 component latency as SOA was decreased, and, across subjects, a positive correlation between the PRP effect and P3 latency lengthening. No SOA-dependent P3 amplitude variation was observed. In experiment 2, the P3 component was measured under single-task conditions. P3 amplitude was higher under single-task than under dual-task conditions, but no SOA-dependent latency variations were observed in this experiment. Overall, the results of both experiments support the notion that part of the processing reflected in P3 activity occurs at or after the locus of the PRP effect, thus suggesting strongly that central mechanisms are involved in P3 latency variations.
Central processing overlap modulates P3 latency
Roberto Dell'Acqua;Francesco Vespignani;
2005
Abstract
Two experiments examined the issue of the functional mechanisms exerting a modulatory effect on the latency of the P3. In experiment 1, using a psychological refractory period (PRP) paradigm, two sequential stimuli (T1 and T2) were presented in each trial at varying stimulus onset asynchronies (SOAs), each requiring a speeded choice response. Substantial lengthening of the reaction time to T2 was observed as SOA decreased (i.e., PRP effect). A systematic investigation of the T2-locked P3 component amplitude and latency was undertaken to discover whether either of these P3 parameters was correlated with the PRP effect. The results showed lengthening of the T2-locked P3 component latency as SOA was decreased, and, across subjects, a positive correlation between the PRP effect and P3 latency lengthening. No SOA-dependent P3 amplitude variation was observed. In experiment 2, the P3 component was measured under single-task conditions. P3 amplitude was higher under single-task than under dual-task conditions, but no SOA-dependent latency variations were observed in this experiment. Overall, the results of both experiments support the notion that part of the processing reflected in P3 activity occurs at or after the locus of the PRP effect, thus suggesting strongly that central mechanisms are involved in P3 latency variations.Pubblicazioni consigliate
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