Generators of the intracranial P50 response in auditory sensory gating

Department of Psychiatry, Wayne State University, 2751 E. Jefferson, Suite 304, Detroit, MI 48207, USA.
NeuroImage (Impact Factor: 6.36). 05/2007; 35(2):814-26. DOI: 10.1016/j.neuroimage.2006.12.011
Source: PubMed

ABSTRACT Clarification of the cortical mechanisms underlying auditory sensory gating may advance our understanding of brain dysfunctions associated with schizophrenia. To this end, data from nine epilepsy patients who participated in an auditory paired-click paradigm during pre-surgical evaluation and had grids of electrodes covering temporal and frontal lobe were analyzed. A distributed source localization approach was applied to the intracranial P50 response and the Gating Difference Wave obtained by subtracting the response to the second stimuli from the response to the first stimuli. Source reconstruction of the P50 showed that the main generators of the response were localized in the temporal lobes. The analysis also suggested that the maximum neuronal activity contributing to the amplitude reduction in the P50 time range (phenomenon of auditory sensory gating) is localized at the frontal lobe. Present findings suggest that while the temporal lobe is the main generator of the P50 component, the frontal lobe seems to be a substantial contributor to the process of sensory gating as observed from scalp recordings.

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    • "in predicting MCI conversion to dementia ( Golob et al . , 2002 , 2007 ) . The P50 is a positive - going wave peaking approximately 50 ms after the onset of an auditory stimulus . It is produced in primary and secondary auditory cortices , though its amplitude is modulated by frontal brain regions and is typically maximal at the vertex electrode ( Korzyukov et al . , 2007 ) . P50 amplitude is influenced primarily by exogenous factors , such as the physical features of a stimulus , rather than by endogenous cognitive factors , such as expectations and evaluation of the environment ( Picton et al . , 1974 ) . P50 amplitude also reflects the inhibition of irrelevant or distracting stimuli , a process known "
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    ABSTRACT: Reductions of cerebrospinal fluid (CSF) amyloid-beta (Aβ42) and elevated phosphorylated-tau (p-Tau) reflect in vivo Alzheimer's disease (AD) pathology and show utility in predicting conversion from mild cognitive impairment (MCI) to dementia. We investigated the P50 event-related potential component as a noninvasive biomarker of AD pathology in non-demented elderly. 36 MCI patients were stratified into amyloid positive (MCI-AD, n=17) and negative (MCI-Other, n=19) groups using CSF levels of Aβ42. All amyloid positive patients were also p-Tau positive. P50s were elicited with an auditory oddball paradigm. MCI-AD patients yielded larger P50s than MCI-Other. The best amyloid-status predictor model showed 94.7% sensitivity, 94.1% specificity and 94.4% total accuracy. P50 predicted amyloid status in MCI patients, thereby showing a relationship with AD pathology versus MCI from another etiology. The P50 may have clinical utility for inexpensive pre-screening and assessment of Alzheimer's pathology. Copyright © 2015. Published by Elsevier B.V.
    Brain research 08/2015; DOI:10.1016/j.brainres.2015.07.054 · 2.84 Impact Factor
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    • "With the current sequential setup, the P50 is most likely a merger of stimulus-driven early and ongoing top-down characteristics (Joos, Gilles, van de Heyning, de Ridder, & Vanneste, 2014; Schwartze et al., 2013). Accordingly, amplitude suppression in response to temporally regular stimulation could be interpreted as an instance of temporal sensory gating, thereby linking the observed phenomenon to P50 suppression obtained with repetitive (gating out) relative to changing (gating in) formal structure in paired stimulus paradigms (Grunwald et al., 2003; Korzyukov et al., 2007). Impairments in sensory gating and temporal processing are both characteristic of schizophrenia but the relation of these aspects and the interplay of formal and temporal predictability remains to be determined in pathological and non-pathological contexts (Allman & Meck, 2012; Allman, Teki, Griffiths, & Meck, 2014; Patterson et al., 2008). "
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    ABSTRACT: To achieve precise timing, the brain needs to establish a representation of the temporal structure of sensory input and use this information to generate timely responses. These operations engage the basal ganglia. Current research in this direction is limited by reliance on animal models, motor and/or offline tasks, small sample sizes, the low temporal resolution of functional magnetic resonance imaging, and the study of progressive neurodegeneration. Here, we combine the excellent temporal resolution of electrophysiological potentials with the high spatial resolution of structural neuroimaging to investigate basal ganglia contributions to sensory timing. Chronic-stage lesion patients and healthy controls listened to pure-tone sequences differing exclusively in temporal regularity. Event-related potentials (ERPs) indicate a selective indifference against this manipulation in patients, attributable to the striatal part of the basal ganglia on the basis of a lesion-mapping approach. These findings provide evidence for a crucial contribution of the basal ganglia to basic sensory functioning. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Cortex 08/2015; 71. DOI:10.1016/j.cortex.2015.07.016 · 5.13 Impact Factor
    • "Furthermore, studies using electroencephalography (EEG), magnetoencephalography (MEG), electrocorticography (ECoG), and fMRI provided some knowledge about brain structures that form the neural network underlying the processing of such auditory stimuli. This network encompasses not only sensory areas, but also areas in the frontal cortex, thalamus, and hippocampus (Grunwald et al., 2003; Thoma et al., 2003; Rosburg et al., 2004; Boutros et al., 2005, 2008; Korzyukov et al., 2007; Kurthen et al., 2007; Tregellas et al, 2007, 2009; Weiland et al., 2008; Mayer et al., 2009; Ji et al., 2013; Bak et al., 2014). However, these studies need to be considered as descriptive rather than as causal. "
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    ABSTRACT: To assess whether the response decrement of auditory evoked potentials (AEPs) after stimulus repetition is affected by an interplay between sensitization and habituation. AEPs were recorded in 18 healthy participants. Stimulation consisted of trains with eight tones. The 6th stimulus of each train was a frequency deviant. The N100 amplitude to the 1st stimulus of the train was quantified in each trial. Trials with initially strong N100 responses and with initially weak N100 responses were averaged separately. For the total trial sample, the N100 and P200 amplitudes decreased from the 1st to the 2nd stimulus of the train but not thereafter. Trials with an initially strong N100 response were qualified by likewise larger N100 amplitudes to the 2nd stimulus, as compared to trials with initially weak N100 responses, and were characterized by a pronounced N100 amplitude decrease from standards to deviants. Our findings are difficult to reconcile with the view that the response decrement of AEP components after stimulus repetition is modulated by sensitization and habituation, as no evidence for either of these two processes could be obtained. The study provides further evidence against habituation as underlying mechanism for the AEP decrement after stimulus repetition. Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
    Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 05/2015; DOI:10.1016/j.clinph.2015.04.071 · 3.10 Impact Factor
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