UNASSIGNED: Dysfunctional sensory gating in anxiety disorders, indexed by the failure to inhibit the P50 event-related potential (ERP) to repeated stimuli, has been linked to deficits in the major inhibitory neurotransmitter γ-aminobutyric acid (GABA).
UNASSIGNED: This study, conducted in 30 healthy volunteers, examined the acute effects of GABAA (lorazepam: 1 mg) and GABAB receptor (baclofen: 10 mg) agonists on P50 measures of auditory sensory gating within a paired-stimulus (S1-S2) paradigm and assessed changes in gating in relation to self-ratings of anxiety.
UNASSIGNED: Compared to placebo, lorazepam reduced ERP indices of sensory gating by attenuating response to S1. Although not directly impacting P50 inhibition, baclofen-induced changes in gating (relative to placebo) were negatively correlated with trait but not state anxiety.
UNASSIGNED: These preliminary findings support the involvement of GABA in sensory gating and tentatively suggest a role for GABAB receptor signaling in anxiety-associated gating dysregulation.

The ameliorating effect of risperidone on apomorphine-induced stereotyped behavior and inhibition of auditory sensory gating was investigated using rhesus monkeys. The total duration of the stereotyped behavior observed in the control group was 43.7 ± 23.0 s (n = 3) between 10 and 25 min after vehicle administration, whereas the duration in the apomorphine-treated (0.1 or 0.15 mg/kg i.m., n = 3) group was observed to be significantly prolonged to 413.0 ± 150.6 s. Administration of 0.01, 0.03, 0.1 mg/kg of risperidone 60 min before apomorphine, significantly reduced the duration of this apomorphine-induced stereotyped behavior to 327 ± 104.9 s (n = 3), 8.3 ± 4.2 s (n = 3), and 0.0 ± × 0.0 s (n = 3, t-test: p < 0.05), respectively. Next, the auditory sensory gating test/conditioning (T/C) ratio was used as a bio-marker. The T/C ratio was 0.598 ± 0.0802 in the vehicle-administered control group (n = 4) and was significantly increased to 2.098 ± 0.254 (n = 4) by apomorphine (0.15 mg/kg, i.m.). Administering of risperidone (0.1 mg/kg, s.c.) 30 min before apomorphine treatment significantly restricted the T/C ratio to 0.571 ± 0.0886 (n = 4), compared to the T/C ratio in the vehicle-administered control group. The above results demonstrate, not only behaviorally but also electrophysiologically, the ameliorating effect of risperidone on the induction of schizophrenia-like symptoms by apomorphine in non-human primates.

Deficits in early auditory sensory processing in schizophrenia have been linked to N-methyl-D-aspartate receptor (NMDAR) hypofunction, but the role of NMDARs in aberrant auditory sensory gating (SG) in this disorder is unclear. This study, conducted in 22 healthy humans, examined the acute effects of a subanesthetic dose of the NMDAR antagonist ketamine on SG as measured electrophysiologically by suppression of the P50 event-related potential (ERP) to the second (S2) relative to the first (S1) of two closely paired (500 ms) identical speech stimuli. Ketamine induced impairment in SG indices at sensor (scalp)-level and at source-level in the auditory cortex (as assessed with eLORETA). Together with preliminary evidence of modest positive associations between impaired gating and dissociative symptoms elicited by ketamine, tentatively support a model of NMDAR hypofunction underlying disturbances in auditory SG in schizophrenia.

Background: While a cochlear implant (CI) can restore access to audibility in deaf children, implanted children may still have difficulty in concentrating. Previous studies have revealed a close relationship between sensory gating and attention. However, whether CI children have deficient auditory sensory gating remains unclear. Methods: To address this issue, we measured the event-related potentials (ERPs), including P50, N100, and P200, evoked by paired tone bursts (S1 and S2) in CI children and normal-hearing (NH) controls. Suppressed amplitudes for S2 compared with S1 in these three ERPs reflected sensory gating during early and later phases, respectively. A Swanson, Nolan, and Pelham IV (SNAP-IV) scale was performed to assess the attentional performance. Results: Significant amplitude differences between S1 and S2 in N100 and P200 were observed in both NH and CI children, indicating the presence of sensory gating in the two groups. However, the P50 suppression was only found in NH children and not in CI children. Furthermore, the duration of deafness was significantly positively correlated with the score of inattention in CI children. Conclusion: Auditory sensory gating can develop but is deficient during the early phase in CI children. Long-term auditory deprivation has a negative effect on sensory gating and attentional performance.

BACKGROUND: Impairment in auditory sensory gating (ASG) has been documented in alcohol dependence [1]. Likewise, it has been shown that ASG becomes abnormal during alcohol administration in otherwise healthy individuals [2]. Patterns of gating abnormality associated with alcohol use are likely associated with an alcohol responsive neurochemical like glutamate (Glu), particularly since it is well-established that alcohol affects NMDA receptors and that glutamatergic functioning is abnormal in both acute alcohol use and in alcohol dependence [3]. Hence, a link between Glu metabolite levels and ASG was hypothesized. It was first hypothesized that Glu and ASG abnormality would be found in groups with alcohol dependence. A second hypothesis was that across groups, greater Glu would predict reduced ASG.
METHODS: Groups were comprised of healthy, non-drinking controls (Controls, N = 4), individuals with current alcohol dependence (AUD-current, N = 6), and with alcohol dependence in remission for at least 1 year (AUD-remission, N = 6). Participants underwent a diagnostic assessment for alcohol consumption, MRI, 1H-MRS for in vivo assessment of Glu and other metabolites, and MEG scanning during a paired click protocol. ASG was computed as the ratio of the source strength of the 50 ms component in the event related field (ERF) to the second click in the pair divided by the source strength of the 50 ms component to the first click in the pair.
RESULTS: Univariate MANOVAs controlling for age and gender revealed a significant effect for group on Glu and ASG, such that ASG ratios were significantly elevated, implying weakened gating. Glu concentration was reduced in AUD-current relative to the other two groups. Further analysis revealed that when additionally controlling for the group effect, reduced Glu predicted increasing impairment in ASG.
CONCLUSIONS: The overall results were consistent with the hypothesis that differences in Glu metabolite levels associated with alcohol dependence result in impaired ASG.

UNASSIGNED: This study aims to investigate the auditory sensory gating capacity in Huffaz using an auditory brainstem response (ABR) test with and without psychological tasks.
UNASSIGNED: Twenty-three participants were recruited for this study. The participants were comprised of 11 Huffaz who memorized 30 chapters of the Islamic Scripture (from the Quran) and 12 non-Huffaz as the control group. All participants had normal hearing perception and underwent an ABR test with and without psychological tasks. The ABR was elicited at 70 dB nHL using a 3000 Hz tone burst stimulus with a 2-0-2 cycle at a stimulus repetition rate of 40 Hz. The ABR wave V amplitude and latencies were measured and statistically compared. A forward digit span test was also conducted to determine participants\' working memory capacity.
UNASSIGNED: There were no significant differences in the ABR wave V amplitudes and latencies between Huffaz and non-Huffaz in ABR with and without psychological tasks. There were also no significant differences in the ABR wave V amplitudes and latencies in both groups of ABR with and without psychological tasks. In addition, no significant differences were identified in the digit span working memory score between both groups.
UNASSIGNED: In this study, based on the ABR findings, Huffaz showed the same auditory sensory gating capacity as the non-Huffaz group. The ABR result was consistent with the digit span working memory test score. This finding implies that both groups have similar working memory performance. However, the conclusion is limited to the specific assessment method that we used in this study.
UNASSIGNED: تهدف هذه الدراسة للتحقق من قدرة البوابات الحسية السمعية لدى الحفاظ باستخدام فحص استجابة جذع الدماغ السمعي مع أو بدون المهام النفسية.
UNASSIGNED: تم اشراك ٢٣ مشاركا في هذه الدراسة. منهم ١١ من الحفاظ الذين يحفظون ٣٠ جزءا من القرآن الكريم و١٢ من غير الحفاظ كمجموعة التحكم. كان لجميع المشاركين إدراك سمع طبيعي وتم إخضاعهم لفحص استجابة جذع الدماغ السمعي مع أو بدون المهام النفسية. تمت استجابة جذع الدماغ السمعي عند ٧٠ ديسيبل باستخدام ٣٠٠٠ هرتز نغمة تحفيز اندفاعية مع ٢-٠-٢ دورة بمعدل تكرار للتحفيز ٤٠ هرتز. كما تم قياس إشارة استجابة جذع الدماغ السمعي سعة ٥ واختفائها ومقارنتها إحصائيا. تم عمل اختبار المدى الرقمي الأمامي لتحديد سعة الذاكرة العاملة للمشاركين.
UNASSIGNED: لم يوجد اختلاف كبير في إشارة استجابة جذع الدماغ السمعي سعة ٥ واختفائها بين الحفاظ وغير الحفاظ في استجابة جذع الدماغ السمعي مع أو بدون المهام النفسية. لم يكن هناك أيضا فرق كبير في إشارة استجابة جذع الدماغ السمعي سعة ٥ واختفائها عند المجموعتين مع أو بدون المهام النفسية. بالإضافة لذلك، لم يلاحظ هناك اختلاف كبير في المدى الرقمي لدرجة الذاكرة العاملة بين المجموعتين.
UNASSIGNED: في هذه الدراسة، اعتمادا على نتائج استجابة جذع الدماغ السمعي، أظهر الحفاظ نفس سعة البوابات الحسية السمعية مثل مجموعة غير الحفاظ. وكانت نتائج استجابة جذع الدماغ السمعي متسقة مع المدى الرقمي لدرجة اختبار الذاكرة العاملة. يعني هذا أن لدى المجموعتين أداء ذاكرة عمل متماثلة. ومع ذلك، النتائج محدودة فقط لطرق التقييم المحددة المستخدمة في هذه الدراسة.

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.

Magnetoencephalography (MEG), a direct measure of neuronal activity, is an underexplored tool in the search for biomarkers of Alzheimer\'s disease (AD). In this study, we used MEG source estimates of auditory gating generators, nonlinear correlations with neuropsychological results, and multivariate analyses to examine the sensitivity and specificity of gating topology modulation to detect AD. Our results demonstrated the use of MEG localization of a medial prefrontal (mPFC) gating generator as a discrete (binary) detector of AD at the individual level and resulted in recategorizing the participant categories in: (1) controls with mPFC generator localized in response to both the standard and deviant tones; (2) a possible preclinical stage of AD participants (a lower functioning group of controls) in which mPFC activation was localized to the deviant tone only; and (3) symptomatic AD in which mPFC activation was not localized to either the deviant or standard tones. This approach showed a large effect size (0.9) and high accuracy, sensitivity, and specificity (100%) in identifying symptomatic AD patients within a limited research sample. The present results demonstrate high potential of mPFC activation as a noninvasive biomarker of AD pathology during putative preclinical and clinical stages. Hum Brain Mapp 38:5180-5194, 2017. © 2017 Wiley Periodicals, Inc.

Auditory sensory gating, assessed in a paired-click paradigm, indicates the extent to which incoming stimuli are filtered, or \"gated\", in auditory cortex. Gating is typically computed as the ratio of the peak amplitude of the event related potential (ERP) to a second click (S2) divided by the peak amplitude of the ERP to a first click (S1). Higher gating ratios are purportedly indicative of incomplete suppression of S2 and considered to represent sensory processing dysfunction. In schizophrenia, hallucination severity is positively correlated with gating ratios, and it was hypothesized that a failure of sensory control processes early in auditory sensation (gating) may represent a larger system failure within the auditory data stream; resulting in auditory verbal hallucinations (AVH). EEG data were collected while patients (N=12) with treatment-resistant AVH pressed a button to indicate the beginning (AVH-on) and end (AVH-off) of each AVH during a paired click protocol. For each participant, separate gating ratios were computed for the P50, N100, and P200 components for each of the AVH-off and AVH-on states. AVH trait severity was assessed using the Psychotic Symptoms Rating Scales AVH Total score (PSYRATS). The results of a mixed model ANOVA revealed an overall effect for AVH state, such that gating ratios were significantly higher during the AVH-on state than during AVH-off for all three components. PSYRATS score was significantly and negatively correlated with N100 gating ratio only in the AVH-off state. These findings link onset of AVH with a failure of an empirically-defined auditory inhibition system, auditory sensory gating, and pave the way for a sensory gating model of AVH.

The stability of cerebral inhibition was assessed across early childhood using a paired-click auditory sensory gating paradigm. The P50 ERP was measured during REM (or its infant analogue, active sleep) and NREM sleep in 14 children at approximately 3 months of age and again at approximately 4 years of age. Evoked response amplitudes, latencies, and the S2/S1 ratio of the amplitudes of the evoked responses were compared between the two visits. Significant reliability was found for the S2/S1 ratio (r = .73, p = .003) during REM but not non REM sleep (r = -.05, p = .88). A significant stimulus number by sleep stage interaction (F(1,12) = 17.1, p = .001) demonstrated that the response to the second stimulus decreased during REM but not NREM sleep. These findings suggest that this measure is stable during REM sleep across early childhood, is not affected by age, and is sleep-state dependent. P50 sensory gating is a biomarker which, if used properly, may provide a mechanism to further explore changes in the developing brain or may help with early screening for psychiatric illness vulnerability.