P50 sensory gating is related to performance on select tasks of cognitive inhibition

Yadon, Carly A.; Bugg, Julie M.; Kisley, Michael A.; Davalos, Deana B.

doi:10.3758/cabn.9.4.448

Cited by 33 publications

(33 citation statements)

References 73 publications

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“…This would not be the case for behaviorally irrelevant (NoGo) stimuli. Supporting this hypothesis, our effect occurred at a latency and locus corresponding to the P50, a component associated with sensory gating mechanisms by which the auditory system prevents irrelevant and/or redundant sensory information from the environment accessing and overwhelming higher-order representations (Hsieh et al, 2004;Kisley et al, 2004;Lijffijt et al, 2009;Yadon et al, 2009). The decrease in response strength of P50 generators associated with learning to respond to Go stimuli may reflect facilitated access for these stimuli to reach higher processing stages.…”

Section: Discussionsupporting

confidence: 62%

Brain Dynamics Underlying Training-Induced Improvement in Suppressing Inappropriate Action

Manuel¹,

Grivel²,

Bernasconi³

et al. 2010

J. Neurosci.

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Inhibitory control, a core component of executive functions, refers to our ability to suppress intended or ongoing cognitive or motor processes. Mostly based on Go/NoGo paradigms, a considerable amount of literature reports that inhibitory control of responses to "NoGo" stimuli is mediated by top-down mechanisms manifesting ϳ200 ms after stimulus onset within frontoparietal networks. However, whether inhibitory functions in humans can be trained and the supporting neurophysiological mechanisms remain unresolved. We addressed these issues by contrasting auditory evoked potentials (AEPs) to left-lateralized "Go" and right NoGo stimuli recorded at the beginning versus the end of 30 min of active auditory spatial Go/NoGo training, as well as during passive listening of the same stimuli before versus after the training session, generating two separate 2 ϫ 2 withinsubject designs. Training improved Go/NoGo proficiency. Response times to Go stimuli decreased. During active training, AEPs to NoGo, but not Go, stimuli modulated topographically with training 61-104 ms after stimulus onset, indicative of changes in the underlying brain network. Source estimations revealed that this modulation followed from decreased activity within left parietal cortices, which in turn predicted the extent of behavioral improvement. During passive listening, in contrast, effects were limited to topographic modulations of AEPs in response to Go stimuli over the 31-81 ms interval, mediated by decreased right anterior temporoparietal activity. We discuss our results in terms of the development of an automatic and bottom-up form of inhibitory control with training and a differential effect of Go/NoGo training during active executive control versus passive listening conditions.

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Section: Discussionsupporting

confidence: 62%

Brain Dynamics Underlying Training-Induced Improvement in Suppressing Inappropriate Action

Manuel¹,

Grivel²,

Bernasconi³

et al. 2010

J. Neurosci.

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“…Deficits in sensory gating are suggested to contribute to disrupted higher-order cognitive processes including attention, working memory and cognitive control (Lijffijt et al, 2009; Smucny et al, 2013; Yadon et al, 2009), and these functions were improved with smoking in patients with schizophrenia (Lohr and Flynn, 1992; Myers et al, 2004; Sacco et al, 2005). Moreover, withdrawal from smoking worsened performance in a visuospatial working memory task in smokers with schizophrenia (George et al, 2002).…”

Section: Resultsmentioning

confidence: 99%

nAChR dysfunction as a common substrate for schizophrenia and comorbid nicotine addiction: Current trends and perspectives

Parikh

Kutlu

Gould

2016

Schizophrenia Research

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Introduction The prevalence of tobacco use in the population with schizophrenia is enormously high. Moreover, nicotine dependence is found to be associated with symptom severity and poor outcome in patients with schizophrenia. The neurobiological mechanisms that explain schizophrenia-nicotine dependence comorbidity are not known. This study systematically reviews the evidence highlighting the contribution of nicotinic acetylcholine receptors (nAChRs) to nicotine abuse in schizophrenia. Methods Electronic data bases (Medline, Google Scholar, and Web of Science) were searched using the selected key words that match the aims set forth for this review. A total of 275 articles were used for the qualitative synthesis of this review. Results Substantial evidence from preclinical and clinical studies indicated that dysregulation of α7 and β2-subunit containing nAChRs account for the cognitive and affective symptoms of schizophrenia and nicotine use may represent a strategy to remediate these symptoms. Additionally, recent meta-analyses proposed that early tobacco use may itself increase the risk of developing schizophrenia. Genetic studies demonstrating that nAChR dysfunction that may act as a shared vulnerability factor for comorbid tobacco dependence and schizophrenia were found to support this view. The development of nAChR modulators was considered an effective therapeutic strategy to ameliorate psychiatric symptoms and to promote smoking cessation in schizophrenia patients. Conclusions The relationship between schizophrenia and smoking is complex. While the debate for the self-medication versus addiction vulnerability hypothesis continues, it is widely accepted that a dysfunction in the central nAChRs represent a common substrate for various symptoms of schizophrenia and comorbid nicotine dependence.

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“…For example, both schizophrenics (Adler et al, 1982; Freedman et al, 1987) and patients suffering from dorsolateral prefrontal cortex lesions (Knight et al, 1999), two populations characterized by high levels of distractibility and noted deficits in attention, exhibit impaired sensory gating. Importantly, an individual’s level of sensory gating has been found to correlate with their performance on certain attention tasks among both patients (Hsieh et al, 2004; Smucny et al, 2013) and healthy controls (Lijffijt et al, 2009a; Yandon et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

Disruption of sensory gating by moderate alcohol doses

Sklar

Nixon

2014

Psychopharmacology

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Rationale Evidence from a growing body of literature suggests that alcohol, even at moderate dose levels, disrupts the ability to ignore distractors. However, little work has been done to elucidate the neural processes underlying this deficit. Objective The present study was conducted to determine if low-to-moderate alcohol doses affect sensory gating, an electrophysiological phenomenon believed to reflect the pre-attentive filtering of irrelevant sensory information. Methods Sixty social drinkers were administered one of three doses intended to produce breath alcohol concentrations of 0.0% (placebo), .04% (i.e., low dose), and .065% (i.e., moderate dose). A paired-click paradigm consisting of 100 pairs of identical tones (S1 and S2) was used to assess sensory gating. Amplitudes of the P50, N100 and P200 auditory evoked potentials (AEPs) were used to calculate gating difference (S1 – S2) and ratio (S2/S1) scores. Results The moderate alcohol dose significantly decreased P50 and N100 gating relative to placebo. Comparisons between the difference and ratio scores helped characterize the gating mechanisms affected at these stages of information processing. Alcohol did not alter P200 sensory gating. Conclusions These data suggest that alcohol disrupts pre-attentional sensory filtering processes at BrACs below the current .08% legal limit. Future studies should perform a combined assessment of sensory gating and selective attention to better understand the relationship between these two alcohol-induced deficits.

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P50 sensory gating is related to performance on select tasks of cognitive inhibition

Cited by 33 publications

References 73 publications

Brain Dynamics Underlying Training-Induced Improvement in Suppressing Inappropriate Action

Brain Dynamics Underlying Training-Induced Improvement in Suppressing Inappropriate Action

nAChR dysfunction as a common substrate for schizophrenia and comorbid nicotine addiction: Current trends and perspectives

Disruption of sensory gating by moderate alcohol doses

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