Recurrent Activity in Higher Order, Modality Non-Specific Brain Regions A Granger Causality Analysis of Autobiographic Memory Retrieval 英文参考文献.docVIP

RecurrentActivityinHigherOrder,ModalityNon- SpecificBrainRegions:AGrangerCausalityAnalysisof AutobiographicMemoryRetrieval HansC.Lou1*,MortenJoensson1,KatjaBiermann-Ruben2,AlfonsSchnitzler2,Leif?stergaard1,TroelsW. Kjaer3,JoachimGross4* 1Center of Functionally Integrative Neuroscience, Aarhus University, Aarhus, Denmark, 2Department of Neurology, Heinrich Heine University, Du¨sseldorf, Germany, 3Department of Clinical Neurophysiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark, 4Department of Psychology, University of Glasgow, Glasgow,UnitedKingdom Abstract It has been proposed that the workings of the brain are mainly intrinsically generated recurrent neuronal activity, with sensory inputs as modifiers of such activity in both sensory and higher order modality non-specific regions. This is supportedbythedemonstrationofrecurrentneuronalactivityinthevisualsystemasaresponsetovisualstimulation.In contrast recurrent activity has never been demonstrated before in higher order modality non-specific regions. Using magneto-encephalography and Granger causality analysis, we tested in a paralimbic network the hypothesis that stimulation may enhance causal recurrent interaction between higher-order, modality non-specific regions. The network includes anterior cingulate/medial prefrontal and posterior cingulate/medial parietal cortices together with pulvinar thalami,anetworkknowntobeeffectiveinautobiographicmemoryretrievalandself-awareness.Autobiographicmemory retrieval of previous personal judgments of visually presented words was used as stimuli. It is demonstrated that the prestimulusconditionischaracterizedbycausal,recurrentoscillationswhicharemaximalinthelowergammarange.When retrievingpreviousjudgmentsofvisuallypresentedadjectives,thisactivityisdramaticallyincreasedduringthestimulustask as ascertained by Granger causality analysis. Our results confirm the hypothesis that stimulation may enhance causal interaction between higher order, modality non-spec