The Experts below are selected from a list of 4731 Experts worldwide ranked by ideXlab platform
Robert Freedman - One of the best experts on this subject based on the ideXlab platform.
-
increased hemodynamic response in the hippocampus thalamus and prefrontal cortex during abnormal Sensory Gating in schizophrenia
Schizophrenia Research, 2007Co-Authors: Jason R Tregellas, Merilyne C. Waldo, Deana B. Davalos, Donald C Rojas, Linzi Gibson, Korey P Wylie, Robert FreedmanAbstract:Abstract Objective Deficits in Sensory Gating are a common feature of schizophrenia. Failure of inhibitory Gating mechanisms, shown by poor suppression of evoked responses to repeated auditory stimuli, has been previously studied using EEG methods. These methods yield information about the temporal characteristics of Sensory Gating deficits, but do not identify brain regions involved in the process. Hence, the neuroanatomical substrates of poor Sensory Gating in schizophrenia remain largely unknown. This study used functional magnetic resonance imaging (fMRI) to investigate the functional neuroanatomy of Sensory Gating deficits in schizophrenia. Methods Twelve patients with schizophrenia and 12 healthy comparison subjects were scanned at 3 Tesla while performing a Sensory Gating task developed for fMRI. P50 EEG evoked potential recordings from a paired-stimulus conditioning-test paradigm were obtained from the same subjects. Results Compared to healthy comparison subjects, patients with schizophrenia exhibited greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex (DLPFC) during the fMRI Sensory Gating task. No group difference was observed in the superior temporal gyrus. Schizophrenia subjects also showed decreased P50 suppression as measured with EEG. Hemodynamic response in the fMRI measure was positively correlated with test/conditioning ratios from the EEG Sensory Gating measure. Conclusions Poor Sensory Gating in schizophrenia is associated with dysfunction of an apparent network of brain regions, including the hippocampus, thalamus and DLPFC. Greater activation of these regions is consistent with evidence for diminished inhibitory function in schizophrenia.
-
Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal Sensory Gating in schizophrenia.
Schizophrenia research, 2007Co-Authors: Jason R Tregellas, Merilyne C. Waldo, Deana B. Davalos, Donald C Rojas, Linzi Gibson, Korey Wylie, Robert FreedmanAbstract:Deficits in Sensory Gating are a common feature of schizophrenia. Failure of inhibitory Gating mechanisms, shown by poor suppression of evoked responses to repeated auditory stimuli, has been previously studied using EEG methods. These methods yield information about the temporal characteristics of Sensory Gating deficits, but do not identify brain regions involved in the process. Hence, the neuroanatomical substrates of poor Sensory Gating in schizophrenia remain largely unknown. This study used functional magnetic resonance imaging (fMRI) to investigate the functional neuroanatomy of Sensory Gating deficits in schizophrenia. Twelve patients with schizophrenia and 12 healthy comparison subjects were scanned at 3 Tesla while performing a Sensory Gating task developed for fMRI. P50 EEG evoked potential recordings from a paired-stimulus conditioning-test paradigm were obtained from the same subjects. Compared to healthy comparison subjects, patients with schizophrenia exhibited greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex (DLPFC) during the fMRI Sensory Gating task. No group difference was observed in the superior temporal gyrus. Schizophrenia subjects also showed decreased P50 suppression as measured with EEG. Hemodynamic response in the fMRI measure was positively correlated with test/conditioning ratios from the EEG Sensory Gating measure. Poor Sensory Gating in schizophrenia is associated with dysfunction of an apparent network of brain regions, including the hippocampus, thalamus and DLPFC. Greater activation of these regions is consistent with evidence for diminished inhibitory function in schizophrenia.
-
P50 Sensory Gating in adolescents from a pacific island isolate with elevated risk for schizophrenia
Biological psychiatry, 2004Co-Authors: Marina Myles-worsley, Lisa M. Ord, Francisca Blailes, Hilda Ngiralmau, Robert FreedmanAbstract:Gating or inhibition of the P50 auditory evoked potential is a heritable neurobiological trait that has shown strong potential to serve as an endophenotype for schizophrenia. P50 Sensory Gating deficits have been found repeatedly in schizophrenic patients and in their unaffected first-degree relatives. P50 Sensory Gating has not yet been studied in high-risk (HR) offspring nor in prodromal adolescents. A paired-stimulus auditory event-related potential paradigm was used to examine P50 Sensory Gating in 44 genetically HR adolescent offspring and 43 clinically HR prodromal adolescents with the same low genetic liability as a comparison group of 39 normal adolescents. Auditory Sensory Gating, as measured by the P50 ratio, was impaired in both genetically HR offspring and also in the clinically HR prodromal adolescents with no close affected relatives. In the genetically HR group, abnormal P50 Sensory Gating was found only in offspring who met criteria for the schizophrenia prodrome. Our findings suggest that P50 deficits are associated with the presence of prodromal symptoms, regardless of genetic risk. The results are consistent with the hypothesis that genetic liability in HR offspring increases risk for prodromal symptoms, and prodromal symptoms, in turn, increase risk for impaired Sensory Gating.
-
p50 Sensory Gating in adolescents from a pacific island isolate with elevated risk for schizophrenia
Biological Psychiatry, 2004Co-Authors: Marina Mylesworsley, Francisca Blailes, Lisa M. Ord, Hilda Ngiralmau, Robert FreedmanAbstract:Abstract Background Gating or inhibition of the P50 auditory evoked potential is a heritable neurobiological trait that has shown strong potential to serve as an endophenotype for schizophrenia. P50 Sensory Gating deficits have been found repeatedly in schizophrenic patients and in their unaffected first-degree relatives. P50 Sensory Gating has not yet been studied in high-risk (HR) offspring nor in prodromal adolescents. Methods A paired-stimulus auditory event-related potential paradigm was used to examine P50 Sensory Gating in 44 genetically HR adolescent offspring and 43 clinically HR prodromal adolescents with the same low genetic liability as a comparison group of 39 normal adolescents. Results Auditory Sensory Gating, as measured by the P50 ratio, was impaired in both genetically HR offspring and also in the clinically HR prodromal adolescents with no close affected relatives. In the genetically HR group, abnormal P50 Sensory Gating was found only in offspring who met criteria for the schizophrenia prodrome. Conclusions Our findings suggest that P50 deficits are associated with the presence of prodromal symptoms, regardless of genetic risk. The results are consistent with the hypothesis that genetic liability in HR offspring increases risk for prodromal symptoms, and prodromal symptoms, in turn, increase risk for impaired Sensory Gating.
-
Early postnatal development of Sensory Gating.
Neuroreport, 2003Co-Authors: Michael A. Kisley, Randal G. Ross, Sherrie D. Polk, Paul M. Levisohn, Robert FreedmanAbstract:Sensory Gating represents the nervous system's ability to inhibit responding to irrelevant environmental stimuli. In order to characterize the early development of acoustic Sensory Gating, suppression of auditory evoked potential component P1 (i.e. P50) in response to paired clicks was measured during REM sleep in healthy infants (1-4 months) that were without genetic risk for disrupted Sensory Gating function (i.e. having a relative with schizophrenia). As a group, the subjects exhibited significant response suppression. A correlation between increasing age and stronger response suppression was uncovered, even within this restricted age range. Parallel changes in sleep physiology could not be ruled out as the explanation for this change. Nevertheless, these results demonstrate that the neural circuits underlying Sensory Gating are functional very early in postnatal development.
Lawrence E. Adler - One of the best experts on this subject based on the ideXlab platform.
-
M50 Sensory Gating predicts negative symptoms in schizophrenia
Schizophrenia Research, 2004Co-Authors: Robert J. Thoma, Faith M. Hanlon, Michael P. Weisend, Mingxiong Huang, Sandra N. Moses, Daniel Ricker, Christopher Edgar, Jessica Irwin, Torres F, Lawrence E. AdlerAbstract:Impaired auditory Sensory Gating is considered characteristic of schizophrenia and a marker of the information processing deficit inherent to that disorder. Predominance of negative symptoms also reflects the degree of deficit in schizophrenia and is associated with poorer pre-morbid functioning, lower IQ, and poorer outcomes. However, a consistent relationship between auditory Sensory Gating and negative symptoms in schizophrenia has yet to be demonstrated. The absence of such a finding is surprising, since both impaired auditory Gating and negative symptoms have been linked with impaired fronto-temporal cortical function. The present study measured auditory Gating using the P50 event related potential (ERP) in a paired-click paradigm and capitalized on the relative localization advantage of magnetoencephalography (MEG) to assess auditory Sensory Gating in terms of the event related field (ERF) M50 source dipoles on bilateral superior temporal gyrus (STG). The primary hypothesis was that there would be a positive correlation between lateralized M50 auditory Sensory Gating measures and negative symptoms in patients with schizophrenia. A standard paired-click paradigm was used during simultaneous EEG and MEG data collection to determine S2/S1 Sensory Gating ratios in a group of 20 patients for both neuroimaging techniques. Participants were administered the Schedule for the Assessment of Negative Symptoms (SANS), the Positive and Negative Symptom Scale (PANSS), and the Calgary Depression Scale for Schizophrenia. Consistent with previous reports, there was no relationship between ERP P50 Sensory Gating and negative symptoms. However, right (not left) hemisphere ERF M50 Sensory Gating ratio was significantly and positively correlated with negative symptoms. This finding is compatible with information processing theories of negative symptoms and with more recent findings of fronto-temporal abnormality in patients with predominantly negative symptoms.
-
Sensory Gating impairment associated with schizophrenia persists into REM sleep
Psychophysiology, 2003Co-Authors: Michael A. Kisley, Sherrie D. Polk, Lawrence E. Adler, Ann Olincy, Merilyne Waldo, Emily Robbins, Robert FreedmanAbstract:Physiological measures of Sensory Gating are increasingly used to study biological factors associated with attentional dysfunction in psychiatric and neurologic patient populations. The present study was designed to assess Sensory Gating during rapid eye movement (REM) sleep in patients with schizophrenia, a population bearing a genetic load for Gating impairment. Auditory event-related potentials (ERPs) were recorded in response to paired clicks during separate waking and overnight sleep recording sessions in controls and schizophrenia patients. Suppression of ERP component P50 was significantly impaired in the patient group during both waking and REM sleep, whereas the difference between groups for N100 Gating was dependent on state. These results suggest that REM sleep is an appropriate state during which to assess P50 Gating in order to disentangle the effects of state and trait on Sensory Gating impairment in other clinical populations.
-
The genetics of Sensory Gating deficits in schizophrenia.
Current psychiatry reports, 2003Co-Authors: Robert Freedman, Lawrence E. Adler, Merilyne C. Waldo, Ann Olincy, Karen E. Stevens, R.g. Ross, Sherry LeonardAbstract:Sensory Gating abnormalities are an early clinical symptom of schizophrenia, and are characterized by a decrease in the brain’s normal ability to inhibit the response to unimportant stimuli. Patients appear hypervigilant and have difficulty focusing their attention. A neurobiologic mechanism involved in these difficulties is nicotinic cholinergic modulation of inhibitory neuronal activity in the hippocampus. One measure of Sensory Gating abnormalities, diminished inhibition of the P50 evoked response to repeated auditory stimuli, has been linked to the chromosome 15q14 locus of the alpha-7-nicotinic receptor gene. This site is one of several that have shown evidence for linkage to schizophrenia, as well as to bipolar disorder, across several studies. Polymorphisms in the core promoter of the gene are associated with schizophrenia and also with diminished inhibition of the P50 response. These genetic data may identify a new pathophysiologic target for drug discovery.
-
Schizophrenia, Sensory Gating, and Nicotinic Receptors
Schizophrenia bulletin, 1998Co-Authors: Lawrence E. Adler, Ann Olincy, Merilyne Waldo, Josette G. Harris, Jay M. Griffith, Karen E. Stevens, Karen A. Flach, Herbert T. Nagamoto, Paula C. Bickford, Sherry LeonardAbstract:A series of human and animal investigations has suggested that altered expression and function of the alpha7-nicotinic cholinergic receptor may be responsible for the auditory Sensory Gating deficit characterized in schizophrenia patients and their relatives as diminished suppression of an auditory-evoked response (P50) to repeated stimuli. This finding, in conjunction with evidence for familial transmission of this Sensory Gating deficit, suggests a pathogenic role of the gene for the alpha7-nicotinic receptor in schizophrenia. This article considers the possible effects of this dysfunction in a broader context. Not only is this dysfunction consistent with difficulties in Sensory Gating, but it might also predispose patients to problems with learning efficiency and accuracy. Such learning problems could underlie schizophrenia patients' delusional thinking, hallucinations, and social dysfunction. In addition, heavy smoking in many schizophrenia patients is consistent with the high concentration of nicotine necessary to activate the receptor and with the receptor's extremely rapid desensitization. Finally, the receptor's possible role in cell growth and differentiation should be considered in connection with developmental deficits and other cellular abnormalities in schizophrenia.
-
Yohimbine impairs P50 auditory Sensory Gating in normal subjects.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 1994Co-Authors: Lawrence E. Adler, Michael A. Kisley, Merilyne Waldo, Herbert T. Nagamoto, Lee Hoffer, Jay M. GiffithAbstract:The evoked response to repeated auditory stimuli generally decreases in amplitude, a phenomenon that demonstrates the activity of Sensory Gating mechanisms in the central nervous system (CNS). Gating of the P50 wave of the auditory evoked response shows such behavior in normals, but not in schizophrenic or manic subjects. In mania, diminished Gating of the auditory evoked response is correlated with elevated levels of noradrenergic metabolites. In animals, yohimbine, a presynaptic alpha-2 antagonist, increases noradrenergic neuronal transmission in the CNS and diminished Gating of the auditory evoked response. The aim of this experiment was to test whether yohimbine causes diminished auditory Sensory Gating in normal human controls. Seven normal subjects with normal P50 auditory Gating were treated either with 0.4 mg/kg of oral yohimbine on one day or placebo on a different day. Each subject acted as his own control. Yohimbine, but not placebo, caused a significant but transient decrease in P50 auditory Gating in these subjects. Thus, increasing CNS noradrenergic neuronal transmission in normal controls can cause a transient impairment in auditory Sensory Gating.
Merilyne C. Waldo - One of the best experts on this subject based on the ideXlab platform.
-
increased hemodynamic response in the hippocampus thalamus and prefrontal cortex during abnormal Sensory Gating in schizophrenia
Schizophrenia Research, 2007Co-Authors: Jason R Tregellas, Merilyne C. Waldo, Deana B. Davalos, Donald C Rojas, Linzi Gibson, Korey P Wylie, Robert FreedmanAbstract:Abstract Objective Deficits in Sensory Gating are a common feature of schizophrenia. Failure of inhibitory Gating mechanisms, shown by poor suppression of evoked responses to repeated auditory stimuli, has been previously studied using EEG methods. These methods yield information about the temporal characteristics of Sensory Gating deficits, but do not identify brain regions involved in the process. Hence, the neuroanatomical substrates of poor Sensory Gating in schizophrenia remain largely unknown. This study used functional magnetic resonance imaging (fMRI) to investigate the functional neuroanatomy of Sensory Gating deficits in schizophrenia. Methods Twelve patients with schizophrenia and 12 healthy comparison subjects were scanned at 3 Tesla while performing a Sensory Gating task developed for fMRI. P50 EEG evoked potential recordings from a paired-stimulus conditioning-test paradigm were obtained from the same subjects. Results Compared to healthy comparison subjects, patients with schizophrenia exhibited greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex (DLPFC) during the fMRI Sensory Gating task. No group difference was observed in the superior temporal gyrus. Schizophrenia subjects also showed decreased P50 suppression as measured with EEG. Hemodynamic response in the fMRI measure was positively correlated with test/conditioning ratios from the EEG Sensory Gating measure. Conclusions Poor Sensory Gating in schizophrenia is associated with dysfunction of an apparent network of brain regions, including the hippocampus, thalamus and DLPFC. Greater activation of these regions is consistent with evidence for diminished inhibitory function in schizophrenia.
-
Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal Sensory Gating in schizophrenia.
Schizophrenia research, 2007Co-Authors: Jason R Tregellas, Merilyne C. Waldo, Deana B. Davalos, Donald C Rojas, Linzi Gibson, Korey Wylie, Robert FreedmanAbstract:Deficits in Sensory Gating are a common feature of schizophrenia. Failure of inhibitory Gating mechanisms, shown by poor suppression of evoked responses to repeated auditory stimuli, has been previously studied using EEG methods. These methods yield information about the temporal characteristics of Sensory Gating deficits, but do not identify brain regions involved in the process. Hence, the neuroanatomical substrates of poor Sensory Gating in schizophrenia remain largely unknown. This study used functional magnetic resonance imaging (fMRI) to investigate the functional neuroanatomy of Sensory Gating deficits in schizophrenia. Twelve patients with schizophrenia and 12 healthy comparison subjects were scanned at 3 Tesla while performing a Sensory Gating task developed for fMRI. P50 EEG evoked potential recordings from a paired-stimulus conditioning-test paradigm were obtained from the same subjects. Compared to healthy comparison subjects, patients with schizophrenia exhibited greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex (DLPFC) during the fMRI Sensory Gating task. No group difference was observed in the superior temporal gyrus. Schizophrenia subjects also showed decreased P50 suppression as measured with EEG. Hemodynamic response in the fMRI measure was positively correlated with test/conditioning ratios from the EEG Sensory Gating measure. Poor Sensory Gating in schizophrenia is associated with dysfunction of an apparent network of brain regions, including the hippocampus, thalamus and DLPFC. Greater activation of these regions is consistent with evidence for diminished inhibitory function in schizophrenia.
-
The genetics of Sensory Gating deficits in schizophrenia.
Current psychiatry reports, 2003Co-Authors: Robert Freedman, Lawrence E. Adler, Merilyne C. Waldo, Ann Olincy, Karen E. Stevens, R.g. Ross, Sherry LeonardAbstract:Sensory Gating abnormalities are an early clinical symptom of schizophrenia, and are characterized by a decrease in the brain’s normal ability to inhibit the response to unimportant stimuli. Patients appear hypervigilant and have difficulty focusing their attention. A neurobiologic mechanism involved in these difficulties is nicotinic cholinergic modulation of inhibitory neuronal activity in the hippocampus. One measure of Sensory Gating abnormalities, diminished inhibition of the P50 evoked response to repeated auditory stimuli, has been linked to the chromosome 15q14 locus of the alpha-7-nicotinic receptor gene. This site is one of several that have shown evidence for linkage to schizophrenia, as well as to bipolar disorder, across several studies. Polymorphisms in the core promoter of the gene are associated with schizophrenia and also with diminished inhibition of the P50 response. These genetic data may identify a new pathophysiologic target for drug discovery.
-
Developmental and genetic influences on the p50 Sensory Gating phenotype
Biological psychiatry, 1996Co-Authors: Marina Myles-worsley, Merilyne C. Waldo, Hilary Coon, William Byerley, David Young, Robert FreedmanAbstract:Evoked potentials to pairs of click stimuli were recorded from 127 subjects ranging in age from 10 to 39 years to examine the developmental course of auditory Sensory Gating. The ratio of the amplitude of the second response to that of the first provides a quantitative measure of auditory Sensory Gating. Contrary to earlier results, the distribution of P50 ratios was unchanged between children and younger adolescents (10-14 years), older adolescents (15-19 years), and adults (20-29 and 30-39 years). Included in the sample were 39 adolescent twins, allowing assessment for possible genetic effects underlying the P50 Sensory Gating phenotype, by comparison of the similarity of the measure in monozygotic and same-sex dizygotic twin pairs. The monozygotic twins had significantly higher similarity for the P50 ratio within each twin pair than the dizygotic twins. These results are consistent with the presence of genetic influences on the P50 Sensory Gating phenotype.
-
Normalization by nicotine of deficient auditory Sensory Gating in the relatives of schizophrenics.
Biological psychiatry, 1992Co-Authors: Lawrence E. Adler, Merilyne C. Waldo, Jay M. Griffith, Lee J. Hoffer, Robert FreedmanAbstract:Diminished Gating of the P50 auditory evoked response to repeated stimuli is a psychophysiological feature of schizophrenia, that is also present in many relatives of patients. Animal models of auditory Sensory Gating indicate that nicotinic cholinergic neurotransmission is a critical neuronal substrate. The aim of this experiment was to determine if the deficit in Sensory Gating could be reversed by nicotine administration. Nonsmoking relatives of schizophrenics with abnormal Sensory Gating were selected as subjects for this initial double-blind trial, to avoid effects of psychotropic medications that might complicate trials in schizophrenic patients themselves. Nicotine-containing gum increased P50 Sensory Gating to near normal levels within 30 min of administration. The effect was transient; the Gating of P50 returned to baseline levels within 1 hr. There was no change observed after placebo administration. In one of the subjects, the anticholinesterase inhibitor physostigmine similarly normalized P50 Gating. The results are consistent with the hypothesis that nicotinic cholinergic neurotransmission may mediate a familial psychophysiological deficit in schizophrenia.
Jürgen Gallinat - One of the best experts on this subject based on the ideXlab platform.
-
P50, N100, and P200 Sensory Gating in Panic Disorder:
Clinical EEG and neuroscience, 2020Co-Authors: Lars Thoma, Johannes Rentzsch, Katharina Gaudlitz, Nicole Tänzer, Jürgen Gallinat, Norbert Kathmann, Andreas Ströhle, Jens PlagAbstract:Panic disorder (PD) has been linked to abnormalities in information processing. However, only little evidence has been published for Sensory Gating in PD. Sensory Gating describes the brain's ability to exclude stimuli of low relevance from higher level information processing, thereby sustaining efficient cognitive processing. Deficits in Sensory Gating have been associated with various psychiatric conditions, most prominently schizophrenia. In this case-control event-related potential study, we tested 32 patients with PD and 39 healthy controls in a double click paradigm. Both groups were compared with regard to pre-attentive (P50), early-attentive (N100), and late-attentive (P200) Sensory Gating indices. Contrary to a hypothesized deficit, PD patients and healthy controls showed no differences in P50, N100 and P200 values. These results suggest that Sensory Gating seems to be functional across the pre-attentive, early-attentive, and late-attentive time span in this clinical population. Given this consistency across auditory Sensory Gating indices, further research aiming to clarify information processing deficits in PD should focus on other neurophysiological markers to investigate information processing deficits in PD (eg, P300, error-related negativity or mismatch negativity).
-
comt val108 158met genotype modulates human Sensory Gating
NeuroImage, 2011Co-Authors: Tomislav Majic, Johannes Rentzsch, Yehonala Gudlowski, Stefan Ehrlich, Georg Juckel, Thomas Sander, Undine E. Lang, Georg Winterer, Jürgen GallinatAbstract:Abstract Background The catechol-O-methyltransferase (COMT) Val 108/158 Met polymorphism of the dopamine system is essential for prefrontal cortex processing capacity and efficiency. In addition, dopaminergic neurotransmission is also associated with the Sensory Gating phenomenon protecting the cerebral cortex from information overload. It is however unclear if COMT genotype as a predictor of prefrontal efficiency modulates Sensory Gating on the level of the auditory cortex, i.e. the Gating of the auditory evoked P50 and N100 components. Methods P50 and N100 Gating and COMT Val 108/158 Met genotype were determined in 282 healthy subjects of German descent carefully screened for psychiatric or neurological disorders. Results A significant effect of the COMT genotype was observed for N100 Gating (F = 4.510, df = 2, p = 0.012) but not for P50 Gating (F = 0.376, df = 2, p = 0.687). Contrast analysis showed that Met/Met individuals had poorer N100 Gating compared to Val/Met (F = − 12.931, p = 0.003) and the Val/Val individuals (F = − 11.056, p = 0.057). Conclusion The results indicate that a high prefrontal efficiency as suggested by the COMT Met/Met genotype is associated with to a poor Sensory Gating of the N100 component. This would fit in a model where a high prefrontal processing capacity allows a pronounced afferent input of Sensory information from the auditory cortex as reflected by a poor Sensory Gating. The more pronounced prefrontal contribution to the N100 compared to the P50 component may explain the exclusive genotype association with the N100 Sensory Gating. This preliminary model should be replicated and validated in future investigations.
-
COMT Val108/158Met genotype modulates human Sensory Gating.
NeuroImage, 2010Co-Authors: Tomislav Majić, Johannes Rentzsch, Yehonala Gudlowski, Stefan Ehrlich, Georg Juckel, Thomas Sander, Undine E. Lang, Georg Winterer, Jürgen GallinatAbstract:The catechol-O-methyltransferase (COMT) Val(108/158)Met polymorphism of the dopamine system is essential for prefrontal cortex processing capacity and efficiency. In addition, dopaminergic neurotransmission is also associated with the Sensory Gating phenomenon protecting the cerebral cortex from information overload. It is however unclear if COMT genotype as a predictor of prefrontal efficiency modulates Sensory Gating on the level of the auditory cortex, i.e. the Gating of the auditory evoked P50 and N100 components. P50 and N100 Gating and COMT Val(108/158)Met genotype were determined in 282 healthy subjects of German descent carefully screened for psychiatric or neurological disorders. A significant effect of the COMT genotype was observed for N100 Gating (F=4.510, df=2, p=0.012) but not for P50 Gating (F=0.376, df=2, p=0.687). Contrast analysis showed that Met/Met individuals had poorer N100 Gating compared to Val/Met (F=-12.931, p=0.003) and the Val/Val individuals (F=-11.056, p=0.057). The results indicate that a high prefrontal efficiency as suggested by the COMT Met/Met genotype is associated with to a poor Sensory Gating of the N100 component. This would fit in a model where a high prefrontal processing capacity allows a pronounced afferent input of Sensory information from the auditory cortex as reflected by a poor Sensory Gating. The more pronounced prefrontal contribution to the N100 compared to the P50 component may explain the exclusive genotype association with the N100 Sensory Gating. This preliminary model should be replicated and validated in future investigations. Copyright © 2010 Elsevier Inc. All rights reserved.
-
Comparison of Midlatency Auditory Sensory Gating at Short and Long Interstimulus Intervals
Neuropsychobiology, 2008Co-Authors: Johannes Rentzsch, Ana Gómez-carrillo De Castro, Andres H. Neuhaus, Maria C. Jockers-scherübl, Jürgen GallinatAbstract:Suppression of P50, N100 and P200 auditory evoked responses in a dual-click procedure is considered an index for the multistage Sensory Gating process. Whereas most studies use a protocol with long interstimulus intervals of 8-12 s between the stimuli pairs, there is also evidence that Sensory Gating occurs at much lower intervals. The aim of the study was to investigate whether a simple modified dual-click protocol with short interstimulus intervals elicts similar Sensory Gating ratios compared to the classic protocol. P50, N100 and P200 amplitudes and Sensory Gating ratios were measured in 23 healthy subjects with 2 different dual-click protocols in 1 session: (1) a simple oddball modified with short interstimulus intervals of about 2.8 s (ISI2), and (2), the classic used with long intervals of about 8 s (ISI8). The amplitudes of the P50, N100 and P200 responses were mostly comparable and correlated between both protocols. Mean Sensory Gating ratios (ISI8/ISI2) were as follows: P50, 35.4/36.4%; N40P50, 36.1/39.9%; N100, 44.4/48.4%; P200, 46.8/43.3%; N100P200, 45.3/41.8%; all differences between protocols, p > 0.1. P50 ratio scores did not show a sufficient correlation between protocols [intraclass correlation coefficient (ICC) P50, 0.13; N40P50, 0.0] compared to N100 (ICC, 0.79), P200 (ICC, 0.6) and N100P200 (ICC, 0.61). Our results contradict the assumption that long interstimulus intervals of about 8 s are absolutely necessary to elicit a marked Sensory Gating phenomenon for P50, N100 and P200 auditory responses (at least when using a protocol with a simple attention task). However, because only healthy subjects were investigated, no prediction can be made for psychiatric patients, in whom neuronal processing may be different. Copyright 2008 S. Karger AG, Basel.
-
Test-retest reliability of P50, N100 and P200 auditory Sensory Gating in healthy subjects.
International journal of psychophysiology : official journal of the International Organization of Psychophysiology, 2007Co-Authors: Johannes Rentzsch, Nash N. Boutros, Maria C. Jockers-scherübl, Jürgen GallinatAbstract:Abstract Rationale Suppression of middle latency auditory evoked responses is considered an index for the multistage Sensory Gating process. This has been observed in sequentially occurring P50, N100 and P200 components in a dual-click procedure. Since P50 Sensory Gating deficits have been observed in schizophrenic patients and first degree relatives, this parameter was suggested as an intermediate phenotype of the disease. However, most studies only show a low reliability for P50 Sensory Gating and neither N100 nor P200 Sensory Gating have been sufficiently tested. Methods Reliability of P50, N100 and P200 Sensory Gating was measured in 41 healthy subjects in two sessions, four weeks apart, using intra-class correlation. Sensory Gating was calculated as ratio-Gating (second response magnitude/first response magnitude × 100) as well as difference-Gating (first response magnitude minus second response magnitude). Results The difference-Gating showed good to excellent reliabilities independently of the amplitude-measurement method applied (P50 peak-to-peak 0.75 and baseline-to-peak 0.74, N100 peak-to-peak 0.63 and baseline-to-peak 0.70, P200 peak-to-peak 0.82 and baseline-to-peak 0.79). Regarding ratio-Gating, best temporal stability was observed for the P200 (peak-to-peak 0.58 and baseline-to-peak 0.62). Reliability of P50 ratio-Gating strongly depends on the amplitude-measurement method (peak-to-peak 0.0 and baseline-to-peak 0.46). Conclusion Regarding long-term reliability in healthy subjects the difference-Gating of all three evoked responses and the ratio-Gating of the P200 component may be useful tools for clinical or intermediate phenotype studies measuring different stages of the auditory Sensory Gating process. In contrast, the reliability of the P50 and N100 ratio-Gating component seems to be insufficient for this purpose. However, long-term reliability remains to be confirmed in clinical samples.
Andreas Von Leupoldt - One of the best experts on this subject based on the ideXlab platform.
-
Being Anxious, Thinking Positively: The Effect of Emotional Context on Respiratory Sensory Gating.
Frontiers in physiology, 2016Co-Authors: Pei-ying S. Chan, Chia-hsiung Cheng, Ya-jhih Jhu, Chia-ling Chen, Andreas Von LeupoldtAbstract:Respiratory Sensory Gating function has been found decreased by induced negative emotion in healthy adults. The increased ratio of the respiratory-related evoked potential (RREP) N1 peak amplitude for the second occlusion (S2) versus the first occlusion (S1), S2/S1, is indicative of such decreased respiratory Sensory Gating. In this study, we tested the hypothesis that a positive emotional context would enhance respiratory Sensory Gating function in healthy individuals. In addition, we tested the modulating role of individual anxiety levels. We compared respiratory Sensory Gating in 40 healthy individuals by the paired inspiratory occlusion paradigm in a positive and neutral emotional context induced by emotional picture viewing. The results showed that the group averaged RREP N1 peak amplitudes S2/S1 ratios were significantly smaller in the positive compared to neutral context (0.49 vs. 0.64; p < .01). Further analysis showed that the ratio decrease was due to a reduced response to the S2 and an enhanced response to S1 in the positive emotional context (p < .05). The subgroup analyses showed that in the positive emotional context, both individuals with low-moderate anxiety levels and those with no anxiety demonstrated a significant decrease of their S2/S1 ratio, but only those with low-moderate anxiety levels showed reduced S2 amplitudes compared to the neutral context (p < .01). In conclusion, our results suggest that a positive emotional context is related to better brain inhibitory mechanisms by filtering out repetitive respiratory stimuli in healthy individuals, especially in the presence of low-moderate anxiety levels. Further investigation on how positive emotional contexts might contribute to improved respiratory Sensory Gating ability in clinical populations is necessary.
-
The Effect of Development in Respiratory Sensory Gating Measured by Electrocortical Activations.
Neural plasticity, 2015Co-Authors: Pei-ying S. Chan, Chia-hsiung Cheng, Andreas Von LeupoldtAbstract:The perception of respiratory sensations can be of significant importance to individuals for survival and greatly impact quality of life. Respiratory Sensory Gating, similar to somatoSensory Gating with exteroceptive stimuli, is indicative of brain cortices filtering out repetitive respiratory stimuli and has been investigated in adults with and without diseases. Respiratory Gating can be tested with the respiratory-related evoked potential (RREP) method in the electroencephalogram with a paired inspiratory occlusion paradigm. Here, the RREP N1 component elicited by the second stimulus (S2) shows reduced amplitudes compared to the RREP N1 component elicited by the first stimulus (S1). However, little is known regarding the effect of development on respiratory Sensory Gating. The present study examined respiratory Sensory Gating in 22 typically developed school-aged children and 22 healthy adults. Paired inspiratory occlusions of 150-ms each with an inter-stimulus-interval of 500-ms were delivered randomly every 2–4 breaths during recording. The main results showed a significantly larger RREP N1 S2/S1 ratio in the children group than in the adult group. In addition, children compared to adults demonstrated significantly smaller N1 peak amplitudes in response to S1. Our results suggest that school-aged children, compared to adults, display reduced respiratory Sensory Gating.
