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This Article Full Text Full Text (PDF) All Versions of this Article: 94/6/4082    most recent 00469.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Ross, B. Articles by Pantev, C. Search for Related Content PubMed PubMed Citation Articles by Ross, B. Articles by Pantev, C.

Stimulus Induced Desynchronization of Human Auditory 40-Hz Steady-State Responses

¹The Rotman Research Institute, Baycrest Centre for Geriatric Care, Toronto, Ontario, Canada; ²Institute for Biomagnetism and Biosignalanalysis, Münster University Hospital, Munich, Germany

Submitted 9 May 2005; accepted in final form 16 August 2005

The hypothesis that gamma-band oscillations are related to the representation of an environmental scene in the cerebral cortex after binding of corresponding perceptual elements is currently under discussion. One question is how the sensory system reacts to a fast change in the scene if perceptual elements are rigidly bound together. A reset of the gamma-band oscillation forced by a change in sensory input may dissolve the binding, which then would be re-established for the new sensation. We studied the reset of gamma-band oscillations on the 40-Hz auditory steady-state responses (ASSR) by means of whole-head magnetoencephalography (MEG). The rhythm of 40-Hz AM of a 500-Hz tone evoked the ASSR, and a short noise burst served as a concurrent stimulus. Possible direct interactions of the auditory stimuli were excluded by presenting the noise impulse in a different frequency channel (2,000–3,000 Hz) to the contralateral ear. The concurrent stimulus induced a considerable decrement in the amplitude of ASSR, which was localized in primary auditory cortices. This decrement lasted 250 ms and was significantly longer than the duration of the transient gamma-band response evoked by the noise burst. Thus it could not be explained by any linear superimposition of the responses. The time courses of ASSR amplitude and phase during recovery from the decrement resembled those after stimulus onset, indicating that a new ASSR was built up after the resetting stimulus. The results are discussed as reset of oscillations in human thalamocortical networks.

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