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Causality in the Association between P300 and Alpha Event-Related Desynchronization
Recent findings indicated that both P300 and alpha event-related desynchronization (α-ERD) were associated, and similarly involved in cognitive brain functioning, e.g., attention allocation and memory updating. However, an explicit causal influence between the neural generators of P300 and α-ERD has...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325251/ https://www.ncbi.nlm.nih.gov/pubmed/22511933 http://dx.doi.org/10.1371/journal.pone.0034163 |
Sumario: | Recent findings indicated that both P300 and alpha event-related desynchronization (α-ERD) were associated, and similarly involved in cognitive brain functioning, e.g., attention allocation and memory updating. However, an explicit causal influence between the neural generators of P300 and α-ERD has not yet been investigated. In the present study, using an oddball task paradigm, we assessed the task effect (target vs. non-target) on P300 and α-ERD elicited by stimuli of four sensory modalities, i.e., audition, vision, somatosensory, and pain, estimated their respective neural generators, and investigated the information flow among their neural generators using time-varying effective connectivity in the target condition. Across sensory modalities, the scalp topographies of P300 and α-ERD were similar and respectively maximal at parietal and occipital regions in the target condition. Source analysis revealed that P300 and α-ERD were mainly generated from posterior cingulate cortex and occipital lobe respectively. As revealed by time-varying effective connectivity, the cortical information was consistently flowed from α-ERD sources to P300 sources in the target condition for all four sensory modalities. All these findings showed that P300 in the target condition is modulated by the changes of α-ERD, which would be useful to explore neural mechanism of cognitive information processing in the human brain. |
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