Sensory Gating Event–Related Potentials and Oscillations in Schizophrenia Patients and Their Unaffected Relatives

Hall, Mei‐Hua; Taylor, Grantley W.; Salisbury, Dean F.; Levy, Deborah L.

doi:10.1093/schbul/sbq027

Cited by 75 publications

(74 citation statements)

References 35 publications

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“…Furthermore, there was a linear relationship between this behavior and coherence in the low-gamma frequency band. Oscillations in the gamma and beta frequency bands have been linked previously to the human sensory gating response (Müller et al, 2001;Johannesen et al, 2005;Hall et al, 2010). Furthermore, both the hippocampus (Zhang et al, 2002) and prefrontal cortex (Mears et al, 2006) have been implicated previously in the PPI response.…”

Section: Prenatal Environmental Insult Results In Changes In Long-ranmentioning

confidence: 88%

Abnormal Long-Range Neural Synchrony in a Maternal Immune Activation Animal Model of Schizophrenia

2010

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The synchrony of neural firing is believed to underlie the integration of information between and within neural networks in the brain. Abnormal synchronization of neural activity between distal brain regions has been proposed to underlie the core symptomatology in schizophrenia. This study investigated whether abnormal synchronization occurs between the medial prefrontal cortex (mPFC) and the hippocampus (HPC), two brain regions implicated in schizophrenia pathophysiology, using the maternal immune activation (MIA) animal model in rats. This neurodevelopmental model of schizophrenia is induced through a single injection of the synthetic immune system activator polyriboinosinic-polyribocytidylic acid, a synthetic analog of double-stranded RNA, a molecular pattern associated with viral infection, in pregnant rat dams. It is based on epidemiological evidence of increased risk of schizophrenia in adulthood after prenatal exposure to infection. In the present study, EEG coherence and neuronal phase-locking to underlying EEG were measured in freely moving MIA and control offspring. The MIA intervention produced significant reductions in mPFC-HPC EEG coherence that correlated with decreased prepulse inhibition of startle, a measure of sensory gating and a hallmark schizotypal behavioral measure. Furthermore, changes in the synchronization of neuronal firing to the underlying EEG were evident in the theta and low-gamma frequencies. Firing within a putative population of theta-modulated, gamma-entrained mPFC neurons was also reduced in MIA animals. Thus, MIA in rats produces a fundamental disruption in long-range neuronal synchrony in the brains of the adult offspring that models the disruption of synchrony observed in schizophrenia.

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Section: Prenatal Environmental Insult Results In Changes In Long-ranmentioning

confidence: 88%

Abnormal Long-Range Neural Synchrony in a Maternal Immune Activation Animal Model of Schizophrenia

2010

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“…This method has been previously established in clinical studies of schizophrenia and autism and to examine power changes in those disorders. To evaluate the state of SNR in this model, baseline, evoked and total power were examined in high and low frequency ranges to determine if these two well established pharmacological models cause perturbations in the noise or stimulus-related signal similar to those found in schizophrenia (Behrendt, 2003; Behrendt and Young, 2004; Brenner et al, 2009; Canive et al, 1998; Dierks et al, 1995; Doheny et al, 2000; Ford et al, 2008; Fujisawa et al, 2004; Gaspar et al, 2009; Hall et al; Hall et al, 2009; Hong et al, 2004; Jensen and Lisman, 1996; Kessler and Kling, 1991; Kirino and Inoue, 1999; Kissler et al, 2000; Koukkou et al, 2000; Krause et al, 2003; Krishnan et al, 2009; Kwon et al, 1999; Leicht et al; Lifshitz et al, 1987; Light et al, 2006; Reinhart et al; Schellenberg and Schwarz, 1993; Spencer et al, 2004; Teale et al, 2008; Yamamoto, 1997). Additionally, inter-trial coherence, a measure for determining the trial to trial response consistency, was examined was analyzed in low and high frequency regions to determine whether or not a loss of response consistency is associated with changes in power.…”

Section: Methodsmentioning

confidence: 99%

NMDA antagonists recreate signal-to-noise ratio and timing perturbations present in schizophrenia

Saunders

Gandal

Siegel

2012

Neurobiology of Disease

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Rationale There is increasing evidence that functional deficits in schizophrenia may be driven by a reduction in the signal-to-noise ratio (SNR) and consistent timing of neural signals. This study examined the extent to which exposure to the NMDA receptor antagonists ketamine and MK801, frequently used pharmacological models of schizophrenia, recreate deficits in electrophysiological markers of disturbed brain circuits that are thought to underlie the illness. Furthermore, this study characterizes the specificity of these differences across the frequency spectrum so as to help identify the nature of selective circuit abnormalities that mediate each oscillatory response as relevant to schizophrenia. Design Mouse EEG was recorded during exposure to repeated auditory stimuli after injection of either vehicle or drug. The dose-response relationship for each electrophysiological measure was determined for ketamine and MK-801. Time-frequency analyses were performed to assess baseline, total, and evoked power and intertrial coherence (ITC) at low (5–10 Hz) and high (35–80 Hz)-frequencies. Results High frequency evoked and total power was decreased by MK-801 and ketamine in a dose-dependent fashion. High frequency baseline power was increased by MK-801 and ketamine in a dose-dependent fashion. Similar to evoked power, high frequency inter-trial coherence was dose-dependently decreased by both drugs. Low frequency ITC was only decreased by ketamine. Conclusions Both ketamine and MK-801 cause alterations in high-frequency baseline (noise), total (signal), and evoked (signal) power resulting in a loss of high frequency SNR that is thought to primarily reflect local circuit activity. These changes indicate an inappropriate increase in baseline activity, which can also be interpreted as non-task related activity. Ketamine induced a loss of intertrial coherence at low frequencies, indicating a loss of consistency in low-frequency circuit mechanisms. As a proportion of baseline power, both drugs had a relative shift from low to high frequencies, reflecting a change in the balance of brain activity from coordination of global regions to a pattern of discoordinated, autonomous local activity. These changes are consistent with a pattern of fragmented regional brain activity seen in schizophrenia.

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“…Indeed, abnormalities have been reported for several frequency bands and have been related to sensory and cognitive functions (Haenschel et al, 2009;Kissler et al, 2000;White et al, 2010). In the paired-stimulus gating design, schizophrenia patients usually display reduced activity in lower frequency bands, whereas alterations in higher frequency bands are less frequently reported (Brenner et al, 2009;Brockhaus-Dumke et al, 2008;Clementz and Blumenfeld, 2001;Edgar et al, 2008;Hall et al, 2010;Hong et al, 2004Hong et al, , 2008Rosburg et al, 2009). These results suggest that a more detailed mapping of the oscillatory activity might help to determine the mechanisms contributing to the P50/M50 gating ratio and its alteration in schizophrenia.…”

Section: Introductionmentioning

confidence: 92%

“…Yet the reason for an exaggerated ratio in schizophrenia remains unclear, and the mechanisms leading to the suppression of the response to S2 are not yet identified. The S2/S1 ratio is potentially sensitive to the encoding processes related to S1 as well as the inhibition processes related to S2, with the relative contributions currently controversial (Clementz and Blumenfeld, 2001;Edgar et al, 2008;Hall et al, 2010;Hong et al, 2004), In particular, it is unclear whether the abnormal gating ratios in schizophrenia reflect dysfunctional encoding, dysfunctional gating, or both.…”

Section: Introductionmentioning

confidence: 99%

Evoked and induced oscillatory activity contributes to abnormal auditory sensory gating in schizophrenia

et al. 2011

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The ratio of magnetoencephalogram-recorded brain responses occurring 50ms after paired clicks (S2-evoked M50/S1-evoked M50) serves as a measure of sensory gating. An abnormally large ratio is commonly found in schizophrenia. Whether this abnormality indicates impaired gating is debated. Using event-related oscillations the present study sought to elucidate processes contributing to the phenomenon of altered M50 gating ratio. Schizophrenia inpatients (n=50) showed the expected large M50 gating ratio relative to 48 healthy controls, which correlated with less induced frontally generated activity in the 10-15Hz frequency band starting 200ms before the onset of S2. Patients also produced smaller alpha (8-12Hz) and gamma (60-80Hz) responses to S1. Results suggest that the deviant gating ratio in schizophrenia is a consequence of a complex alteration in the processing of incoming information that cannot be attributed to impaired gating alone.

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Sensory Gating Event–Related Potentials and Oscillations in Schizophrenia Patients and Their Unaffected Relatives

Cited by 75 publications

References 35 publications

Abnormal Long-Range Neural Synchrony in a Maternal Immune Activation Animal Model of Schizophrenia

Abnormal Long-Range Neural Synchrony in a Maternal Immune Activation Animal Model of Schizophrenia

NMDA antagonists recreate signal-to-noise ratio and timing perturbations present in schizophrenia

Evoked and induced oscillatory activity contributes to abnormal auditory sensory gating in schizophrenia

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