Paired-click Paradigm Research Articles

The Effect of Attention on Auditory Processing in Adults on the Autism Spectrum.

This study examined the effect of attention on auditory processing in autistic individuals. Electroencephalography data were recorded during two attention conditions (passive and active) from 24 autistic adults and 24 neurotypical controls, ages 17-30 years. The passive condition involved only listening to the clicks and the active condition involved a button press following single clicks in a modified paired-click paradigm. Participants completed the Adolescent/Adult Sensory Profile and the Social Responsiveness Scale 2. The autistic group showed delayed N1 latencies and reduced evoked and phase-locked gamma power compared to neurotypical peers across both clicks and conditions. Longer N1 latencies and reduced gamma synchronization predicted greater social and sensory symptoms. Directing attention to auditory stimuli may be associated with more typical neural auditory processing in autism.

Examining the impact of schizotypal personality traits on event-related potential (ERP) indexes of sensory gating in a healthy population.

The aim of this study was to better understand the relation of schizotypy traits with sensory gating ability in a sample of community-dwelling individuals with high and low schizotypy traits. Sensory gating was assessed through the paired click paradigm and mid-latency evoked responses (i.e., P50, N100, P200), while schizotypy traits were assessed through the SPQ-BR which was used to classify participants into "high" and "low" schizotypy groups. Based on prior work, we hypothesized that those with the highest schizotypy scores would have reduced sensory gating ability. While this study does not show differences between relatively low and high schizotypy groups on sensory gating ability, it does suggest that our participants may have been experiencing deficits in attention allocation, a downstream cognitive processing measure. Scores on the SPQ-BR suggest that our sample was not close to the high end of the schizotypy traits which may help explain why no differences were found. This research shows the importance of including all levels of schizotypy ratings in clinical research as we can gain a clearer view of the impact of schizotypy on the brain and cognitive functioning in those with "high" levels of schizotypy. Additionally, this work highlights the importance of including measures of important factors such as impulsivity and sensation-seeking to better understand what aspects of schizotypy may be driving these sensory gating alterations reported in the literature.

Short-term transcutaneous trigeminal nerve stimulation does not affect visual oddball task and paired-click paradigm ERP responses in healthy volunteers

Recent research suggests that transcutaneous trigeminal nerve stimulation (TNS) may positively affect cognitive function. However, no clear-cut evidence is available yet, since the majority of it derives from clinical studies, and the few data on healthy subjects show inconsistent results. In this study, we report the effects of short-term TNS on event-related potentials (ERP) recorded during the administration of a simple visual oddball task and a paired-click paradigm, both considered useful for studying brain information processing functions. Thirty-two healthy subjects underwent EEG recording before and after 20min of sham- or real-TNS, delivered bilaterally to the infraorbital nerve. The amplitude and latency of P200 and P300 waves in the simple visual oddball task and P50, N100 and P200 waves in the paired-click paradigm were measured before and after treatment. Our results show that short-term TNS did not alter any of the ERP parameters measured, suggesting that in healthy subjects, short-term TNS may not affect brain processes involved in cognitive functions such as pre-attentional processes, early allocation of attention and immediate memory. The perspective of having an effective, non-pharmacological, non-invasive, and safe treatment option for cognitive decline is particularly appealing; therefore, more research on the positive effects on cognition of TNS is definitely needed.

Acute Stress and Gender Effects in Sensory Gating of the Auditory Evoked Potential in Healthy Subjects.

Sensory gating is a neurophysiological measure of inhibition that is characterized by a reduction in the P50, N100, and P200 event-related potentials to a repeated identical stimulus. It was proposed that abnormal sensory gating is involved in the neural pathological basis of some severe mental disorders. Since then, the prevailing application of sensory gating measures has been in the study of neuropathology associated with schizophrenia and so on. However, sensory gating is not only trait-like but can be also state-like, and measures of sensory gating seemed to be affected by several factors in healthy subjects. The objective of this work was to clarify the roles of acute stress and gender in sensory gating. Data showed acute stress impaired inhibition of P50 to the second click in the paired-click paradigm without effects on sensory registration leading to worse P50 sensory gating and disrupted attention allocation reflected by attenuated P200 responses than control condition, without gender effects. As for N100 and P200 gating, women showed slightly better than men without effects of acute stress. Data also showed slightly larger N100 amplitudes across clicks and significant larger P200 amplitude to the first click for women, suggesting that women might be more alert than men.

LEDA-Localized-EEG Dynamics Analyzer: a MATLAB-Based Innovative Toolbox for Analysis of EEG Source Dynamics

Establishing conclusive cortical activity dynamics from neuroimages and high dimensional neuronal data post-processing, such as scalp-EEG/ERP or its localized source data, is always challenging. For addressing this, we introduce LEDA, localized-EEG dynamics analyzer, offering our novel techniques, namely (1)the localized source activity to duration (LSAD) ratio that elegantly combines voxel activation with temporal information enabling a spatiotemporal condition comparison, (2)cortical region’s activation-duration summary generation, (3)anatomical dominance calculator, and (4)voxel activations’ GIF animation extraction feature. They effectively explore and quantify physiological spatiotemporal dynamics and provide insights more intuitive than EEG/ERP biomarkers. To demonstrate, we chose to study sensory gating deficits in schizophrenia for which the P50 wave biomarker is widely discussed. EEG response (64 channels@1 kHz) to auditory paired-click paradigm from 9 patients and 9 controls was processed to ERP. Source localization was achieved by using sLORETA, a widely-used source reconstruction algorithm. LSAD ratio of patients significantly differed from that of controls for the auditory cortical regions (p value < 0.05). It revealed that inhibitory alpha activity pattern was prominent in parietal, temporal and occipital lobe for controls and not patients. Conversely, the frontal lobe, specifically the middle frontal gyrus, was temporally the most active analogously across all subjects. LEDA also extracted that swift alpha activity exists between 100 and 300 ms time period. These derived results match with existing fMRI studies, speak beyond P50 wave suppression biomarker and emphasize that our methods successfully uncovered meaningful brain mechanisms at high spatiotemporal resolution. They are provided as an open-source MATLAB based toolbox for applicability to other neuronal pathological investigations.

Expanding our understanding of sensory gating in children with autism spectrum disorders

ObjectiveThis study examined sensory gating in children with autism spectrum disorders (ASD). Gating is usually examined at the P50 component and rarely at mid- and late-latency components. MethodsElectroencephalography data were recorded during a paired-click paradigm, from 18 children with ASD (5–12 years), and 18 typically-developing (TD) children. Gating was assessed at the P50, N1, P2, and N2 event-related potential components. Parents of all participants completed the Short Sensory Profile (SSP). ResultsTD children showed gating at all components while children with ASD showed gating only at P2 and N2. Compared to TD children, the ASD group showed significantly reduced gating at P50, N1, and P2. No group differences were found at N2, suggesting typical N2 gating in the ASD group. Time-frequency analyses showed reduced orientation and neural synchronization of auditory stimuli. P50 and N1 gating significantly correlated with the SSP. ConclusionAlthough children with ASD have impaired early orientation and filtering of auditory stimuli, they exhibited gating at P2 and N2 components suggesting use of different gating mechanisms compared to TD children. Sensory deficits in ASD may relate to gating. SignificanceThe data provide novel evidence for impaired neural orientation, filtering, and synchronization in children with ASD.

P50, N100, and P200 Auditory Sensory Gating Deficits in Schizophrenia Patients.

BackgroundSensory gating describes neurological processes of filtering out redundant or unnecessary stimuli during information processing, and sensory gating deficits may contribute to the symptoms of schizophrenia. Among the three components of auditory event-related potentials reflecting sensory gating, P50 implies pre-attentional filtering of sensory information and N100/P200 reflects attention triggering and allocation processes. Although diminished P50 gating has been extensively documented in patients with schizophrenia, previous studies on N100 were inconclusive, and P200 has been rarely examined. This study aimed to investigate whether patients with schizophrenia have P50, N100, and P200 gating deficits compared with control subjects.MethodsControl subjects and clinically stable schizophrenia patients were recruited. The mid-latency auditory evoked responses, comprising P50, N100, and P200, were measured using the auditory-paired click paradigm without manipulation of attention. Sensory gating parameters included S1 amplitude, S2 amplitude, amplitude difference (S1-S2), and gating ratio (S2/S1). We also evaluated schizophrenia patients with PANSS to be correlated with sensory gating indices.ResultsOne hundred four patients and 102 control subjects were examined. Compared to the control group, schizophrenia patients had significant sensory gating deficits in P50, N100, and P200, reflected by larger gating ratios and smaller amplitude differences. Further analysis revealed that the S2 amplitude of P50 was larger, while the S1 amplitude of N100/P200 was smaller, in schizophrenia patients than in the controls. We found no correlations between sensory gating indices and schizophrenia positive or negative symptom clusters. However, we found a negative correlation between the P200 S2 amplitude and Bell’s emotional discomfort factor/Wallwork’s depressed factor.ConclusionTill date, this study has the largest sample size to analyze P50, N100, and P200 collectively by adopting the passive auditory paired-click paradigm without distractors. With covariates controlled for possible confounds, such as age, education, smoking amount and retained pairs, we found that schizophrenia patients had significant sensory gating deficits in P50-N100-P200. The schizophrenia patients had demonstrated a unique pattern of sensory gating deficits, including repetition suppression deficits in P50 and stimulus registration deficits in N100/200. These results suggest that sensory gating is a pervasive cognitive abnormality in schizophrenia patients that is not limited to the pre-attentive phase of information processing. Since P200 exhibited a large effect size and did not require additional time during recruitment, future studies of P50-N100-P200 collectively are highly recommended.

The Influence of Background Auditory Noise on P50 and N100 Suppression Elicited by the Paired-Click Paradigm

Abstract. Auditory sensory gating is commonly assessed using the Paired-Click Paradigm (PCP), an electroencephalography (EEG) task in which two identical sounds are presented sequentially and the brain’s inhibitory response to the second sound is measured. Many clinical populations demonstrate reduced P50 and/or N100 suppression. Testing sensory gating in children may help to identify individuals at risk for neurodevelopmental disorders earlier, including autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), which could lead to more optimal outcomes. Minimal research has been done with children because of the difficulty of performing lengthy EEG experiments with young children, requiring them to sit still for long periods of time. We designed a modified, potentially child-friendly version of the PCP and evaluated it in typically developing adults. The PCP was administered twice, once in a traditional silent room (silent movie condition) and once with an audible movie playing (audible movie condition) to minimize boredom and enhance behavioral compliance. We tested whether P50 and N100 suppression were influenced by the presence of the auditory background noise from the movie. N100 suppression was observed in both hemispheres in the silent movie condition and in the left hemisphere only during the audible movie condition, though suppression was attenuated in the audible movie condition. P50 suppression was not observed in either condition. N100 sensory gating was successfully elicited with an audible movie playing during the PCP, supporting the use of the modified task for future research in both children and adults.

Dysfunction of Inferior Parietal Lobule During Sensory Gating in Patients With Amnestic Mild Cognitive Impairment.

Patients with amnestic mild cognitive impairment (aMCI) demonstrate significant cognitive deficits, especially in the memory aspect. The memory deficiency might be attributed to the difficulties in the inhibitory function to suppress redundant stimuli. Sensory gating (SG) refers to the attenuation of neural responses to the second identical stimulus in a paired-click paradigm, in which auditory stimuli are delivered in pairs with inter-stimulus intervals (ISI) of 500 ms and inter-pair intervals of 6–8 s. It is considered as an electrophysiological signal to reflect the brain’s automatic response to gate out repetitive sensory inputs. However, there has been no study systematically investigating SG function in aMCI patients. Thus, the present study used magnetoencephalography (MEG) to record neuromagnetic responses to a paired-click paradigm in 23 healthy controls (HC) and 26 aMCI patients. The Stimulus 2/Stimulus 1 (S2/S1) amplitude ratio was used to represent the SG function. Compared to HC, aMCI patients showed M50 SG deficits in the left inferior frontal gyrus (IFG) and right inferior parietal lobule (IPL). M100 SG defects were also observed in the right IPL. Based on the ROIs showing significant between-group SG differences, we found that a more deficient M50 SG function in the right IPL was associated with poorer performance in the immediate recall of Logic Memory (LM), Chinese Version Verbal Learning Test (CVVLT) and Digit Span Backward (DSB) Test. Furthermore, the M50 SG ratios of the right IPL together with the neuropsychological performance of LM and CVVLT demonstrated very good accuracy in the discrimination of aMCI from HC. In conclusion, compared to HC, aMCI patients showed a significant SG deficit in the right IPL, which was correlated with the auditory short-term memory function. We suggest the combination of SG in the right IPL, LM and CVVLT to be sensitive indicators to differentiate aMCI patients from HC.

Abnormal beta and gamma frequency neural oscillations mediate auditory sensory gating deficit in schizophrenia

BackgroundSensory gating is a process in which the brain's response to irrelevant and repetitive stimuli is inhibited. The sensory gating deficit in schizophrenia (SZ) is typically measured by the ratio or difference score of the P50 event-related potential (ERP) amplitudes in response to a paired click paradigm. While the P50 gating effect has usually been measured in relation to the peak amplitude of the S1 and S2 P50 ERPs, there is increasing evidence that inhibitory processes may be reflected by evoked or induced oscillatory activity during the inter-click interval in the beta (20–30 Hz) and gamma (30–50 Hz) frequency bands. We therefore examined the relationship between frequency specific activity in the inter-click interval with gating effects in the time and frequency domains. MethodPaired-auditory stimuli were presented to 131 participants with schizophrenia and 196 healthy controls (HC). P50 ERP amplitudes to S1 and S2as well as averaged- and single-trial beta (20–30 Hz) and gamma (30–50 Hz) frequency power during the inter-click interval were measured from the CZ electrode site. ResultsIn the time domain, P50 gating deficits were apparent in both ratio and difference scores. This effect was mainly due to smaller S1 amplitudes in the patient group. SZ patients exhibited less evoked beta and gamma power, particularly at the 0–100 ms time point, in response to S1. Early (0–100 ms) evoked beta and gamma responses were critical in determining the S1 amplitude and extent of P50 gating across the delay interval for both HC and SZ. ConclusionOur findings support a disruption in initial sensory registration in those with SZ, and do not support an active mechanism throughout the delay interval. The degree of response to S1 and early beta and gamma frequency oscillations in the delay interval provides information about the mechanisms supporting auditory sensory gating, and may provide a framework for studying the mechanisms that support sensory inhibition.

Effect of alpha-NETA on auditory event related potentials in sensory gating study paradigm in mice

The potential contribution of trace amines (TA) to the pathophysiology of neuropsychiatric disorders makes it interesting to examine the effect of TA receptor ligands on schizophrenia biomarkers. We studied the effect of systemic administration of a putative Trace Amine-Associated Receptor 5 (TAAR5) agonist, alpha-NETA (2-(alpha-naphthoyl) ethyltrimethylammonium iodide), on the amplitude of the N40 event related potentials component and on the sensory gating (SG) index in C57BL/6 mice. It was found that low doses of alpha-NETA (2.5 mg/kg and 5 mg/kg) do not elicit a significant effect on the parameters of the N40 component and the SG index. However, the higher dose of alpha-NETA (10 mg/kg) induces a significant effect on the N40 component, but since a decrease in amplitude is observed on both the first and second stimuli in the pair, the SG index does not change. Thus, alpha-NETA administration causes a steady decrease in the N40 amplitude in response to both the first and second stimuli in the paired-click paradigm, and an increase in the N40 peak latency.

P50-N100-P200 sensory gating deficits in adolescents and young adults with autism spectrum disorders

Sensory symptoms are common in individuals with autism spectrum disorder (ASD). Altered sensory gating may cause sensory overload. However, whether ASD individuals have P50 gating deficits is controversial in childhood and lacks evidence in adulthood. Beyond P50, fewer studies have examined N100 or P200, although N100 is considered to be more reliable than P50. Also, the clinical correlates of these parameters are mostly unknown. This study aimed to investigate P50, N100, and P200 sensory gating in adolescents and young adults with ASD and examine their clinical correlates. In a sample of 34 ASD participants (mean age 20.6 ± 4.1, female 5.9%) and 34 sex- and age-matched typically-developing controls (TDC, mean age 20.4 ± 3.1), we investigated P50, N100, and P200 sensory gating by a paired-click paradigm, which generated the data of S1 amplitude after the first click and S2 amplitude after the second click. We found that compared to TDC, ASD participants had significant N100 suppression deficits reflected by a larger N100 S2 amplitude, smaller N100 ratio of S2 over S1, and the difference between the two amplitudes. N100 S2 amplitude was significantly associated with sensory sensitivity independent of the diagnosis. Although there was no group difference in P50 suppression, S1 amplitude was negatively associated with social deficits in ASD. P200 gating parameters were correlated with attention switching difficulty. Our findings suggest N100 gating deficit in adolescents and young adults with ASD. The relationships between P50 S1 and social deficits and between N100 S2 and sensory sensitivity warrant further investigation.

Attention modulates topology and dynamics of auditory sensory gating.

This work challenges the widely accepted model of sensory gating as a preattention inhibitory process by investigating whether attention directed at the second tone (S2) within a paired-click paradigm could affect gating at the cortical level. We utilized magnetoencephalography, magnetic resonance imaging and spatio-temporal source localization to compare the cortical dynamics underlying gating responses across two conditions (passive and attention) in 19 healthy subjects. Source localization results reaffirmed the existence of a fast processing pathway between the prefrontal cortex (PFC) and bilateral superior temporal gyri (STG) that underlies the auditory gating process. STG source dynamics comprised two gating sub-components, Mb1 and Mb2, both of which showed significant gating suppression (>51%). The attention directed to the S2 tone changed the gating network topology by switching the prefrontal generator from a dorsolateral location, which was active in the passive condition (18/19), to a medial location, active in the attention condition (19/19). Enhanced responses to the attended stimulus caused a significant reduction in gating suppression in both STG gating components (>50%). Our results demonstrate that attention not only modulates sensory gating dynamics, but also exerts topological rerouting of information processing within the PFC. The present data, suggesting that the cortical levels of early sensory processing are subject to top-down influences, change the current view of gating as a purely automatic bottom-up process.

Evoked Potentials Investigations of Deficit Versus Nondeficit Schizophrenia: EEG-MEG Preliminary Data.

Heterogeneity of schizophrenia is a major obstacle toward understanding the disorder. One likely subtype is the deficit syndrome (DS) where patients suffer from predominantly negative symptoms. This study investigated the evoked responses and the evoked magnetic fields to identify the neurophysiological deviations associated with the DS. Ten subjects were recruited for each group (Control, DS, and Nondeficit schizophrenia [NDS]). Subjects underwent magnetoencephalography (MEG) and electroencephalography (EEG) testing while listening to an oddball paradigm to generate the P300 as well as a paired click paradigm to generate the mid-latency auditory-evoked responses (MLAER) in a sensory gating paradigm. MEG-coherence source imaging (CSI) during P300 task revealed a significantly higher average coherence value in DS than NDS subjects in the gamma band (30-80 Hz), when listening to standard stimuli but only NDS subjects had a higher average coherence level in the gamma band than controls when listening to the novel sounds. P50, N100, and P3a ERP amplitudes (EEG analysis) were significantly decreased in NDS compared with DS subjects. The data suggest that the deviations in the 2 patient groups are qualitatively different. Deviances in NDS patients suggest difficulty in both early (as in the gating paradigm), as well as later top-down processes (P300 paradigm). The main deviation in the DS group was an exaggerated responsiveness to ongoing irrelevant stimuli detected by EEG whereas NDS subjects had an exaggerated response to novelty.

Forward masking recovery in bottlenose dolphins (Tursiops truncatus): Auditory brainstem responses to paired-click stimuli in high-pass masking noise

Adaptation is a fundamental process in the auditory system and underlies the automatic gain control system of echolocating bottlenose dolphins. As pulse-echo delay increases, auditory brainstem response (ABR) amplitudes to the echoes progressively increase. This study examined adaptation across cochlear frequency regions using a paired-click (i.e., forward masking) paradigm and high-pass masking noise. Bottlenose dolphins passively listened to paired click stimuli (20–160 kHz “pink” spectra). A “conditioning” click was followed by a “probe” click with equal amplitude and a time delay ranging from 125 to 750 μs. ABRs to click pairs were obtained with and without high-pass masking noise that precluded the basal turn of the cochlea from responding to the click stimuli. The ABR evoked by a single click (temporally aligned with the first click of the paired-click condition) was subtracted from the click-pair ABR to visualize the response evoked by the probe click. Probe ABR amplitudes recovered linearly with increasing delay relative to the conditioning click, and were approximately 70% of full response amplitude at 750-μs delay. Paired-click interval ABR amplitude recovery functions were similar for the unmasked and high-pass masked conditions. [Work sponsored by ONR.]

Auditory N100 gating in patients with schizophrenia: A systematic meta-analysis

ObjectiveThe study sought to assess the presence of auditory N100 gating deficits in patients with schizophrenia by meta-analysis. MethodsLiterature was screened for studies on patients with schizophrenia that used the paired-click paradigm and reported N100 data. Both electroencephalographic and magnetoencephalographic studies were considered. N100 gating measures as well as the N100 amplitudes to the initial and repeated stimulus were extracted and subjected to a meta-analysis. ResultsThe literature research revealed 29 studies, reporting either N100 gating or N100 amplitude measures in paired-click experiments. Patients with schizophrenia exhibited less N100 gating than healthy controls across studies (mean g = −0.405, SE = 0.051). However, what appeared as a gating deficit in patients was due to reduced N100 amplitudes to the initial stimulus in this group (mean g = 0.610, SE = 0.075). Patients and controls did not differ in their N100 amplitudes to the repeated stimulus (mean g = 0.042, SE = 0.066). ConclusionThere is no evidence for an auditory N100 gating deficit in schizophrenia, but for an impaired N100 response recovery. SignificancePrevious findings on impaired N100 gating in schizophrenia patients reflect deficient processing of auditory salience rather than defective inhibition of repeating redundant auditory stimulation.

Sensory Gating Deficits and their Clinical Correlates in Drug-Free/Drug-Naive Patients with Schizophrenia.

Background:Sensory gating refers to “filtering” of irrelevant sensory input in the brain. Auditory sensory gating deficit has been considered as a marker of schizophrenia (SCZ) and assessed using P50 paired-click paradigm. We explore sensory gating deficits and their clinical correlates in SCZ.Materials and Methods:Twenty-five drug-free/drug-naïve patients with SCZ, whose psychopathology was assessed using Positive and Negative Syndrome Scale (PANSS), and 25 age-matched normal controls (NC) were recruited. ERP recordings were done using 40-channel event-related potential measuring system.Results:S2-S1 P50 amplitude difference, an index of sensory gating, was significantly lower in SCZ at F3 and F4 sites when compared to NC, indicating impaired gating. SCZ had significantly lower S1 amplitude compared to NC at these sites; S2 amplitudes were comparable. The sensory gating index also showed significant correlations with PANSS scores.Conclusions:Our study reiterates sensory gating abnormalities in SCZ and confers a frontal specificity, implying specific deficits in early preattentive processes to them. Further, we suggest that gating deficits in SCZ are driven predominantly by abnormally small S1 rather than an inability to suppress S2. A correlation between sensory gating parameters and measures of psychopathology strengthens the hypothesis that abnormal response to sensory input may contribute to the psychopathology in SCZ.

F207. SCHIZOTYPY AND SENSORY GATING: A 6-MONTH-OLD EEG STUDY

BackgroundSchizotypal traits are present in the general population and are distributed along a continuum, with the clinical disorder schizophrenia found at its extremity (Claridge, 1997). Schizotypy is a dimension of personality within the general population, which has been found to be elevated among schizophrenia-spectrum patients (Brosey and Woodward, 2015) and their first-degree relatives (Morenzo-Izco et al., 2015). One hypothesis to account for the sensory deficits observed across the spectrum suggests a difficulty in the inhibition of irrelevant sensory input, such as the secondary beep in the paired-click paradigm.Sensory gating describes the pre-attentional habituation of responses to repeated sensory input, for example, auditory tones. This gating mechanism is used to distinguish between important and irrelevant information (Hall et al., 2011) and is typically explored using the paired-click paradigm and analysed using the P50 event-related potential component. This can be observed approximately 50-milliseconds following the presentation of an auditory stimulus and is a highly established biological trait of schizophrenia, with abnormalities displayed in the P50 component all throughout the schizophrenia-spectrum.MethodsThis research aimed to observe whether the 6-month-old offspring of mothers with schizotypic traits display abnormalities in the P50 event-related component when explored using the paired-click paradigm. The paired-click paradigm was used to highlight the sensory-gating abilities of fifty-three 6-month-old infants during 15-minutes of continuous sleep. The mothers of the infants completed the Short Form of the Oxford and Liverpool Inventory of Feelings and Experiences, which was used to determine their personality dimension scores, and identify schizotypic traits. Participants were categorized into one of three groups: infants of controls mothers, infants of intermediate mothers, and infants of schizotypic mothers.ResultsIt was predicted that the 6-month-old infants of mothers who demonstrate schizotypy scores would demonstrate different amplitudes compared to those of control mothers. This research found a significant generalized difference between the P50 component for the paired-clicks in the right hemisphere of the brain (F(1,51)=5.34, p=.025), and a significant latency effect was observed in the frontal regions (F(1,51)=5.41, p=.024). A significant between-subjects effect was observed centrally (F(2,50)=3.71, p=.031); suggesting there are significant differences between the ways each group distinguished the paired-clicks. Infants of schizotypic mothers showed an increase in activation compared to other groups. An interaction was observed in the left hemisphere between the paired-clicks and each identifiable group (F(2,50) = 3.45, p = .039). In addition to the P50 a significant slow wave effect was also observed across the left (F(1,51)=8.38, p=.006) and right (F(1,51)=7.81, p=.007) posterior regions; a latency effect in the left (F(1,51)=5.47, p=.023), and a distinction in mean amplitude in the right (F(1,51)=7.25, p=.010).DiscussionSchizotypy is viewed as a risk factor for schizophrenia, which is present in the general population, and is present on the schizophrenia-spectrum. The 6-month-old infants of mothers showed an increase in activity centrally, demonstrating that the infants’ P50 amplitudes were influenced by their mothers’ schizotypy status. This finding is consistent with the developmental hypothesis of schizophrenia, however longitudinal studies will be required to determine whether a sensory gating deficit is a valid predictor of the later onset of schizophrenia.

Maternal deprivation induces alterations in cognitive and cortical function in adulthood

Early life trauma is a risk factor for a number of neuropsychiatric disorders, including schizophrenia (SZ). The current study assessed how an early life traumatic event, maternal deprivation (MD), alters cognition and brain function in rodents. Rats were maternally deprived in the early postnatal period and then recognition memory (RM) was tested in adulthood using the novel object recognition task. The expression of catechol-o-methyl transferase (COMT) and glutamic acid decarboxylase (GAD67) were quantified in the medial prefrontal cortex (mPFC), ventral striatum, and temporal cortex (TC). In addition, depth EEG recordings were obtained from the mPFC, vertex, and TC during a paired-click paradigm to assess the effects of MD on sensory gating. MD animals exhibited impaired RM, lower expression of COMT in the mPFC and TC, and lower expression of GAD67 in the TC. Increased bioelectric noise was observed at each recording site of MD animals. MD animals also exhibited altered information theoretic measures of stimulus encoding. These data indicate that a neurodevelopmental perturbation yields persistent alterations in cognition and brain function, and are consistent with human studies that identified relationships between allelic differences in COMT and GAD67 and bioelectric noise. These changes evoked by MD also lead to alterations in shared information between cognitive and primary sensory processing areas, which provides insight into how early life trauma confers a risk for neurodevelopmental disorders, such as SZ, later in life.

TAAR5 receptor agonist affects sensory gating in rats

Trace amines are structurally close to classical monoamines and dysregulation in trace amines and/or their receptors might contribute to pathology of mental disorders. The study was aimed to investigate the effect of recently identified Trace Amine-Associated Receptor 5 (TAAR5) agonist 2-(alpha-naphthoyl)ethyltrimethylammonium iodide (alpha-NETA) on sensory gating (SG) in awake freely moving rats. SG was studied in paired-click paradigm and SG index was calculated as difference in event related potentials component N40 amplitudes to the first and second stimulus in the pair. The 1 mg/kg dose of alpha-NETA as well as the control injection of saline had no significant effects on the SG index. However, higher doses of alpha-NETA (3 and 5 mg/kg) significantly decreased the SG index. The change in the SG index was mainly due to a decrease in the N40 amplitude, and the 5 mg/kg dose caused the N40 decrease both in response to the first and second stimulus in the pair. Thus, TAAR5 activation can influence SG, indicating the potential role of trace amines and TAAR5 in sensory information dosing.