Test–retest reliability of P50, N100 and P200 auditory sensory gating in healthy subjects

Rentzsch, Johannes; Jockers-Scherübl, Maria C.; Boutros, Nash N.; Gallinat, Jürgen

doi:10.1016/j.ijpsycho.2007.10.006

Cited by 122 publications

(77 citation statements)

References 83 publications

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“…Although P50 amplitudes were not altered by DAT1 polymorphisms, our preliminary findings indicated that P50 suppression, indexed by dP50, tended to be greater in 9R (vs. 10R) individuals during placebo treatment, and was found to be reduced in this same allele group with nicotine (vs. placebo) administration. The notoriously low reliability of the ratio gating (rP50) index may have contributed to its insensitivity to allele type and nicotine, while the relatively higher reliability of dP50 would have maintained suppressor classification across treatment sessions and provided more stability for detecting acute responsiveness to a test dose of nicotine (Rentzsch et al, 2008).These preliminary findings extend results of previous studies reporting a baselinedependency of pharmacologically altered neural and cognitive activity that has been ascribed to inter-individual quantitative variations in synaptic dopamine. Observations that dopamine agonists either improve or impair brain processes have been accounted for by using the inverted-U principle, that is, agonists might stimulate the dopamine system to 'optimal' or overdosed levels in individuals with low and high baseline dopamine system functioning, respectively (Cools, 2008;Cools and Robbins, 2004).…”

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confidence: 69%

Section: Discussionmentioning

confidence: 99%

“…In addition to the peak amplitude and latency (i.e. time of peak P50 relative to stimulus onset) of S 1 -and S 2 -P50, two auditory gating indixes were derived for each recording: (a) rP50, measured as the amplitude of S 2 -P50 divided by S 1 -P50 amplitude, ×100; (b) dP50, which is the most reliable (relative to rP50) gating index (Fuerst et al, 2007;Rentzsch et al, 2008), was measured as the mathematical difference score derived by subtracting the amplitude of S 2 -P50 from S 1 -P50 amplitude. …”

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The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine

et al. 2011

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Although schizophrenia has been considered primarily a disease of dopaminergic neurotransmission, the role of dopamine in auditory sensory gating deficits in this disorder and their amelioration by smoking/nicotine is unclear. Hypothesizing that individual differences in striatal dopamine levels may moderate auditory gating and its modulation by nicotine, this preliminary study used the mid-latency (P50) auditory event-related potential (ERP) to examine the single dose (6 mg) effects of nicotine (vs. placebo) gum on sensory gating in 24 healthy nonsmokers varying in the genetic expression of the dopamine transporter (DAT). Consistent with an inverted-U relationship between dopamine level and the drug effects, individuals carrying the 9R (lower gene expression) allele, which is related to greater striatal dopamine levels, tended to evidence increased baseline gating compared to 10R (higher gene expression) allele carriers and showed a reduction in gating with acute nicotine. The present results may help to understand the link between excessive smoking and sensory gating deficits in schizophrenia and to explain the potential functional implications of genetic disposition on nicotinic treatment in schizophrenia. Keywords schizophrenia; P50; gating; dopamine transporter gene; nicotine; smoking Early theoretical models of information processing in schizophrenia postulated impairment in the preattentive, automatic processing of sensory input to be a contributing factor in the appearance of psychotic symptoms, perceptual disturbances, and various cognitive deficits that characterize this disorder (Venables, 1964). Meta-analyses and reviews of event-related potential (ERP) studies probing auditory sensory gating in a paired stimulus paradigm (involving the presentation two [ CIHR Author Manuscript CIHR Author Manuscript CIHR Author Manuscriptfound that ~90% of patients with schizophrenia as well as ~50% of their first-degree relatives exhibit insufficient inhibitory processing of repetitive, irrelevant acoustic stimuli (Bramon et al., 2004;De Wilde et al., 2007;Patterson et al., 2008). Typically assessed with the amplitude of the early (50 ms) positive ERP component, P50, abnormal auditory sensory gating has been evidenced by a relative inability to suppress P50 to S 2 , and is expressed by larger S 2 /S 1 ratio (rP50) and/or smaller S 1 minus S 2 difference (dP50) scores.Smoking and acute nicotine have transiently corrected deficient P50 processing in schizophrenia patients and their relatives, respectively (Adler et al., 1992(Adler et al., , 1993. In addition, in a rodent model of schizophrenia-like gating deficiency, studies assessing the P20-N40 ERP, which is an analogue of the human P50, have shown agonists and antagonists of the α7 nicotinic receptor to improve deficient S 2 inhibition and to block normal S 2 inhibition, respectively (Stevens et al., 1998(Stevens et al., , 1999Simosky et al., 2001). Other studies reporting gating improvements with nicotine in rodents and humans, however, have found increa...

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confidence: 69%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine

et al. 2011

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“…In psychiatry, a number of attempts have been made to develop and determine the feasibility of candidate endophenotypes, but few have met all the criteria listed above. For instance, modern brain imaging tools present problems with retest stability, and the heritability of brain activation (deficits) has only rarely been demonstrated [4,5] . However, modern imaging techniques do provide more insight into pathophysiological mechanisms and thus advance our understanding of the biological underpinnings of psychotic symptoms.…”

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confidence: 99%

Genes and Neuroimaging: Advances in Psychiatric Research

Gallinat¹,

Bauer²,

Heinz³

2008

Neurodegener Dis

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Major psychiatric disorders, including schizophrenia, bipolar disorder and substance addiction, are partly heritable and show a multifactorial pattern of heredity. Although the introduction of explicit diagnostic criteria has improved clinical research on psychiatric disorders, the concept is only of limited use for exploring their genetic underpinnings. On the behavioral level, psychopathological symptoms can hardly separate the many pathophysiological subgroups. Contrary to nosological categories, biologically based phenotypes – referred to as intermediate phenotypes – consisting of neuropsychological, electrophysiological, functional and structural brain imaging parameters, could represent the genetic basis more directly. Thus intermediate phenotypes are being targeted in current molecular genetic investigations. In this article, we review existing data on the effects of genetic variation in the dopamine and serotonin systems (catechol-O-methyltransferase, the serotonin-transporter-linked polymorphic region) on the morphometric, metabolic and functional characteristics of the cerebral cortex and limbic structures. The gene-driven modulation of these brain circuits is discussed with regard to their behavioral correlates and their role for psychiatric diseases. Furthermore, recently identified putative susceptibility genes for schizophrenia (neuregulin 1, dysbindin, G72) are briefly discussed.

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“…Last, and maybe most important, it has been shown that P50 gating has a limited retestreliability. 28 Further supporting this idea, there is a wide range of P50 gating values reported in the literature for both schizophrenia patients and healthy subjects, 29 and many studies failed to find a significantly reduced P50 ratio in schizophrenia patients compared with healthy controls. [30][31][32][33][34][35] Problems with test-retest reliability have been noted frequently, especially with ratio values that introduce a disadvantageous signal-to-noise ratio to both the numerator and the denominator.…”

Section: Discussionmentioning

confidence: 94%

Critical Evaluation of Auditory Event-Related Potential Deficits in Schizophrenia: Evidence From Large-Scale Single-Subject Pattern Classification

Neuhaus

Popescu

Rentzsch

et al. 2013

Schizophrenia Bulletin

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Event-related potential (ERP) deficits associated with auditory oddball and click-conditioning paradigms are among the most consistent findings in schizophrenia and are discussed as potential biomarkers. However, it is unclear to what extend these ERP deficits distinguish between schizophrenia patients and healthy controls on a single-subject level, which is of high importance for potential translation to clinical routine. Here, we investigated 144 schizophrenia patients and 144 matched controls with an auditory click-conditioning/oddball paradigm. P50 and N1 gating ratios as well as target-locked N1 and P3 components were submitted to conventional general linear models and to explorative machine learning algorithms. Repeatedmeasures ANOVAs revealed significant between-group differences for the oddball-locked N1 and P3 components but not for any gating measure. Machine learning-assisted analysis achieved 77.7% balanced classification accuracy using a combination of target-locked N1 and P3 amplitudes as classifiers. The superiority of machine learning over repeated-measures analysis for classifying schizophrenia patients was in the range of about 10% as quantified by receiver operating characteristics. For the first time, our study provides large-scale single-subject classification data on auditory click-conditioning and oddball paradigms in schizophrenia. Although our study exemplifies how automated inference may substantially improve classification accuracy, our data also show that the investigated ERP measures show comparably poor discriminatory properties in single subjects, thus illustrating the need to establish either new analytical approaches for these paradigms or other paradigms to investigate the disorder.

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Test–retest reliability of P50, N100 and P200 auditory sensory gating in healthy subjects

Cited by 122 publications

References 83 publications

The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine

The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine

Genes and Neuroimaging: Advances in Psychiatric Research

Critical Evaluation of Auditory Event-Related Potential Deficits in Schizophrenia: Evidence From Large-Scale Single-Subject Pattern Classification

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