Literature DB >> 16376575

Modulation of spectral power and of phase resetting of EEG contributes differentially to the generation of auditory event-related potentials.

Ll Fuentemilla1, J Marco-Pallarés, C Grau.   

Abstract

Nowadays, the mechanisms involved in the genesis of event-related potentials (ERPs) are a matter of debate among neuroscientists. Specifically, the debate lies in whether ERPs arise due to the contribution of a fixed-polarity and fixed-latency superimposed neuronal activity to background electroencephalographic oscillations (evoked model) and/or due to a partial phase synchronization of the ongoing EEG (oscillatory model). The participation of the two mechanisms can be explored by the spectral power modulation and phase coherence of scalp EEG rhythms, respectively. However, an important limitation underlies their measurement: the fact that an added neural activity will be relatively phase-locked to stimulus, thus enhancing both spectral power and phase synchrony measures and making the contribution of each mechanism less clear-cut. This would not be relevant in the case that an increase in phase concentration was not accompanied by any concurrent spectral power modulation, thus opening the way to an oscillatory-based explanation. We computed event-related spectral power modulations and phase coherence to an auditory repeated-stimulus presentation paradigm with tone intensity far from threshold (90 dB SPL), in which N1 decreases its amplitude (N1 gating) as an attenuation brain process. Our data indicate that evoked and oscillatory activity could contribute together to the non-attenuated N1, while N1 to repeated stimuli could be explained by partial phase concentration of scalp EEG activity without concurrent power increase. Therefore, our results show that both increased spectral power and partial phase resetting contribute differentially to different ERPs. Moreover, they show that certain ERPs could arise through reorganization of the phase of ongoing scalp EEG activity only.

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Year:  2006        PMID: 16376575     DOI: 10.1016/j.neuroimage.2005.10.036

Source DB:  PubMed          Journal:  Neuroimage        ISSN: 1053-8119            Impact factor:   6.556


  28 in total

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