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


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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    • "Furthermore, developmental changes within the prefrontal cortex that lead to changes in attentional control may result in sensory gating improvements with age (Knight, Staines, Swick, & Chao, 1999; Marshall, Bar-Haim, & Fox, 2004). Further support for top-down influences on sensory gating has emerged from ERP studies which have found significant correlations between measures of frontal lobe dysfunction and sensory gating (Boutros et al., 2009), as well as P50 generators within the frontal lobes (Grunwald et al., 2003; Korzyukov et al., 2007; Liu, Xiao, Shi, & Zhao, 2011; Mears, Klein, & Cromwell, 2006). "

    Full-text · Article · Oct 2016 · Brain and Cognition
    • "Thirdly, although neural correlates of P50 SG have been largely explored (Boutros, Gjini, Eickhoff, Urbach, & Pflieger, 2013; Grunwald et al., 2003; Korzyukov et al., 2007), knowledge about the circuitry of N100 SG remains poorly understood. While bilateral temporal regions have been considered as main neural generators of auditory P50/N100 SG, recent functional magnetic resonance imaging and event-related potential (ERP) studies disclosed the frontal/prefrontal contribution in paired-stimulus or short-term habituation paradigms (Grau, Fuentemilla, & Marco- Pallares, 2007; Grunwald et al., 2003; Korzyukov et al., 2007; Mayer et al., 2009; Oranje, Aggernaes, Rasmussen, Ebdrup, & Glenthoj, 2013; Weiland, Boutros, Moran, Tepley, & Bowyer, 2008; Weisser et al., 2001). In addition, there is ample behavioral and neuroimaging evidence supporting the hypothesis of frontal aging, which postulates frontal/prefrontal cortex is particularly vulnerable to physiological aging (Tisserand & Jolles, 2003; West, 1996). "
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    ABSTRACT: Aging has been associated with declines in sensory-perceptual processes. Sensory gating (SG), or repetition suppression, refers to the attenuation of neural activity in response to a second stimulus and is considered to be an automatic process to inhibit redundant sensory inputs. It is controversial whether SG deficits, as tested with an auditory paired-stimulus protocol, accompany normal aging in humans. To reconcile the debates arising from event-related potential studies, we recorded auditory neuromagnetic reactivity in 20 young and 19 elderly adult men and determined the neural activation by using minimum-norm estimate (MNE) source modeling. SG of M100 was calculated by the ratio of the response to the second stimulus over that to the first stimulus. MNE results revealed that fronto-temporo-parietal networks were implicated in the M100 SG. Compared to the younger participants, the elderly showed selectively increased SG ratios in the anterior superior temporal gyrus, anterior middle temporal gyrus, temporal pole and orbitofrontal cortex, suggesting an insufficient age-related gating to repetitive auditory stimulation. These findings also highlight the loss of frontal inhibition of the auditory cortex in normal aging.
    No preview · Article · Oct 2015 · Brain and Cognition
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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.
    Full-text · Article · Aug 2015 · Brain research
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