The modulatory influence of a predictive cue on the auditory steady-state response.
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ABSTRACT:
SUBMITTER: Weisz N
PROVIDER: S-EPMC6869987 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The Auditory Steady-State Response (ASSR) in the electroencephalogram (EEG) is usually reduced in schizophrenia (SZ), particularly to 40 Hz stimulation. The gamma frequency ASSR deficit has been attributed to N-methyl-D-aspartate receptor (NMDAR) hypofunction. We tested whether the NMDAR antagonist, phencyclidine (PCP), produced similar ASSR deficits in rats. EEG was recorded from awake rats via intracranial electrodes overlaying the auditory cortex and at the vertex of the skull. ASSRs to click trains were recorded at 10, 20, 30, 40, 50, and 55 Hz and measured by ASSR Mean Power (MP) and Phase Locking Factor (PLF). In Experiment 1, the effect of different subcutaneous doses of PCP (1.0, 2.5 and 4.0 mg/kg) on the ASSR in 12 rats was assessed. In Experiment 2, ASSRs were compared in PCP treated rats and control rats at baseline, after acute injection (5 mg/kg), following two weeks of subchronic, continuous administration (5 mg/kg/day), and one week after drug cessation. Acute administration of PCP increased PLF and MP at frequencies of stimulation below 50 Hz, and decreased responses at higher frequencies at the auditory cortex site. Acute administration had a less pronounced effect at the vertex site, with a reduction of either PLF or MP observed at frequencies above 20 Hz. Acute effects increased in magnitude with higher doses of PCP. Consistent effects were not observed after subchronic PCP administration. These data indicate that acute administration of PCP, a NMDAR antagonist, produces an increase in ASSR synchrony and power at low frequencies of stimulation and a reduction of high frequency (> 40 Hz) ASSR activity in rats. Subchronic, continuous administration of PCP, on the other hand, has little impact on ASSRs. Thus, while ASSRs are highly sensitive to NMDAR antagonists, their translational utility as a cross-species biomarker for NMDAR hypofunction in SZ and other disorders may be dependent on dose and schedule.
| S-EPMC4530939 | biostudies-literature
Project description:Deviant auditory steady-state responses (aSSRs) in the gamma range (30-90?Hz) may be translational biomarkers for schizophrenia (SZ). This study tests whether aSSR deviations are (i) specific to SZ across the psychosis dimension, (ii) specific to particular frequency bands, and (iii) present in bipolar I disorder without psychosis (BDNP). METHODS:Beta (20-), low- (40-), and high-gamma (80-Hz) aSSRs were measured with EEG and compared across 113 SZ, 105 schizoaffective disorder (SAD), 99 bipolar disorder with psychosis (BDP), 68 BDNP, and 137 healthy comparison subjects (HC). Standard aSSR measures (single-trial power [STP] and inter-trial phase coherence [ITC]), as well as evoked responses to stimulus onsets/offsets and pre-stimulus power, were quantified. Multivariate canonical discriminant analysis was used to summarize variables that efficiently and maximally differentiated groups. RESULTS:(i) Psychosis groups showed reduced responses on ITC 20?Hz, STP/ITC 40?Hz, STP/ITC 80?Hz, indicating dimensional reductions in aSSR across the psychosis spectrum not specific to aSSR frequency. For the 40- and 80-Hz ITCs there was greater reduction in SZ compared to SAD, possibly indexing cortical disruptions linked to psychosis without mood symptoms. (ii) All probands had elevated pre-stimulus power, possibly compromising neural entrainment to the steady-state stimuli. (iii) Onset/Offset and 80?Hz ITC responses were most important for group discrimination and showed dimensional reduction across the schizo-bipolar spectrum. CONCLUSIONS:Deviant aSSRs were found across the schizo-bipolar spectrum at multiple frequencies with psychosis status and severity linked to greatest reductions at low and high gamma.
| S-EPMC6661193 | biostudies-literature
Project description:An aided sound-field auditory steady-state response (ASSR) has the potential to be used to objectively validate hearing-aid (HA) fittings in clinics. Each aided ear should ideally be tested independently, but it is suspected that binaural testing may be used by clinics to reduce test time. This study simulates dichotic ASSR sound-field conditions to examine the risk of making false judgments due to unchecked binaural effects. Unaided ASSRs were recorded with a clinical two-channel electroencephalography (EEG) system for 15 normal hearing subjects using a three-band CE-Chirp® stimulus. It was found that the noise corrected power of a response harmonic can be suppressed by up to 10 dB by introducing large interaural time differences equal to half the time period of the stimulus envelope, which may occur in unilateral HA users. These large interaural time differences also changed the expression of ASSR power across the scalp, resulting in dramatically altered topographies. This would lead to considerably lower measured response power and possibly nondetections, evidencing that even well fit HAs are fit poorly (false referral), whereas monaural ASSR tests would pass. No effect was found for simulated lateralizations of the stimulus, which is beneficial for a proposed aided ASSR approach. Full-scalp ASSR recordings match previously found 40 Hz topographies but demonstrate suppression of cortical ASSR sources when using stimuli in interaural envelope antiphase.
| S-EPMC8580520 | biostudies-literature
Project description:Background:The 22q11.2 deletion syndrome confers a markedly increased risk for schizophrenia. 22q11.2 deletion carriers without manifest psychotic disorder offer the possibility to identify functional abnormalities that precede clinical onset. Since schizophrenia is associated with a reduced cortical gamma response to auditory stimulation at 40 Hz, we hypothesized that the 40 Hz auditory steady-state response (ASSR) may be attenuated in nonpsychotic individuals with a 22q11.2 deletion. Methods:Eighteen young nonpsychotic 22q11.2 deletion carriers and a control group of 27 noncarriers with comparable age range (12-25 years) and sex ratio underwent 128-channel EEG. We recorded the cortical ASSR to a 40 Hz train of clicks, given either at a regular inter-stimulus interval of 25 ms or at irregular intervals jittered between 11 and 37 ms. Results:Healthy noncarriers expressed a stable ASSR to regular but not in the irregular 40 Hz click stimulation. Both gamma power and inter-trial phase coherence of the ASSR were markedly reduced in the 22q11.2 deletion group. The ability to phase lock cortical gamma activity to regular auditory 40 Hz stimulation correlated with the individual expression of negative symptoms in deletion carriers (? = -0.487, P = .041). Conclusions:Nonpsychotic 22q11.2 deletion carriers lack efficient phase locking of evoked gamma activity to regular 40 Hz auditory stimulation. This abnormality indicates a dysfunction of fast intracortical oscillatory processing in the gamma-band. Since ASSR was attenuated in nonpsychotic deletion carriers, ASSR deficiency may constitute a premorbid risk marker of schizophrenia.
| S-EPMC5815132 | biostudies-literature
Project description:Auditory evoked steady-state responses are increasingly being used as a marker of brain function and dysfunction in various neuropsychiatric disorders, but research investigating the test-retest reliability of this response is lacking. The purpose of this study was to assess the consistency of the auditory steady-state response (ASSR) across sessions. Furthermore, the current study aimed to investigate how the reliability of the ASSR is impacted by stimulus parameters and analysis method employed. The consistency of this response across two sessions spaced approximately 1 week apart was measured in nineteen healthy adults using electroencephalography (EEG). The ASSR was entrained by both 40 Hz amplitude-modulated white noise and click train stimuli. Correlations between sessions were assessed with two separate analytical techniques: a) channel-level analysis across the whole-head array and b) signal-space projection from auditory dipoles. Overall, the ASSR was significantly correlated between sessions 1 and 2 (p<0.05, multiple comparison corrected), suggesting adequate test-retest reliability of this response. The current study also suggests that measures of inter-trial phase coherence may be more reliable between sessions than measures of evoked power. Results were similar between the two analysis methods, but reliability varied depending on the presented stimulus, with click train stimuli producing more consistent responses than white noise stimuli.
| S-EPMC3899078 | biostudies-literature
Project description:Auditory selective attention enables task-relevant auditory events to be enhanced and irrelevant ones suppressed. In the present study we used a frequency tagging paradigm to investigate the effects of attention on auditory steady state responses (ASSR). The ASSR was elicited by simultaneously presenting two different streams of white noise, amplitude modulated at either 16 and 23.5 Hz or 32.5 and 40 Hz. The two different frequencies were presented to each ear and participants were instructed to selectively attend to one ear or the other (confirmed by behavioral evidence). The results revealed that modulation of ASSR by selective attention depended on the modulation frequencies used and whether the activation was contralateral or ipsilateral. Attention enhanced the ASSR for contralateral activation from either ear for 16 Hz and suppressed the ASSR for ipsilateral activation for 16 Hz and 23.5 Hz. For modulation frequencies of 32.5 or 40 Hz attention did not affect the ASSR. We propose that the pattern of enhancement and inhibition may be due to binaural suppressive effects on ipsilateral stimulation and the dominance of contralateral hemisphere during dichotic listening. In addition to the influence of cortical processing asymmetries, these results may also reflect a bias towards inhibitory ipsilateral and excitatory contralateral activation present at the level of inferior colliculus. That the effect of attention was clearest for the lower modulation frequencies suggests that such effects are likely mediated by cortical brain structures or by those in close proximity to cortex.
| S-EPMC4205007 | biostudies-literature
Project description:Background:Paired associative stimulation (PAS) is the repeated combination of a sensory stimulus with transcranial magnetic stimulation (TMS) in close temporal association. Recently, a study demonstrated that PAS of an auditory stimulus together with TMS of the temporal cortex is capable of changing the amplitude of auditory evoked potentials (AEP). Objective:This study examined the influence of tone duration and habituation in temporal cortex PAS as elicited by 40 and 20?Hz amplitude modulated auditory steady-state responses (aSSR). Methods:Eighteen subjects participated in two experiments, including two PAS protocols each, which consisted of 200 auditory stimuli (4?kHz) paired with temporal cortex TMS with an interstimulus interval (ISI) of 45?ms between tone onset and TMS pulse, delivered at 0.1?Hz. Experiment 1 compared auditory stimuli with different lengths [PAS (23?ms) vs. PAS (400?ms)]. Experiment 2 investigated verum vs. sham PAS. aSSR for the paired tone (4?kHz) and a control tone (1?kHz) were measured pre- and post-interventional-using 40?Hz aSSR in experiment 1 and both 20 and 40?Hz aSSR in experiment 2. Results:A statistically significant, sham-controlled decrease in amplitude was observed for the 20?Hz aSSR using the 4?kHz PAS carrier frequency in experiment 2. Conclusion:Frequency-specific effects for the 20?Hz aSSR confirm the feasibility of auditory PAS and highlight the secondary auditory cortex as its target site, introducing new possible treatment protocols for patients suffering from tinnitus. The amplitude decrease can be explained by principles of spike timing-dependent plasticity and the superposition model of aSSR.
| S-EPMC5682298 | biostudies-literature
Project description:Schizophrenia patients exhibit dysfunctional gamma oscillations in response to simple auditory stimuli or more complex cognitive tasks, a phenomenon explained by reduced NMDA transmission within inhibitory/excitatory cortical networks. Indeed, a simple steady-state auditory click stimulation paradigm at gamma frequency (~40 Hz) has been reproducibly shown to reduce entrainment as measured by electroencephalography (EEG) in patients. However, some investigators have reported increased phase locking factor (PLF) and power in response to 40 Hz auditory stimulus in patients. Interestingly, preclinical literature also reflects this contradiction. We investigated whether a graded deficiency in NMDA transmission can account for such disparate findings by administering subanesthetic ketamine (1-30 mg/kg, i.v.) or vehicle to conscious rats (n=12) and testing their EEG entrainment to 40 Hz click stimuli at various time points (~7-62 min after treatment). In separate cohorts, we examined in vivo NMDA channel occupancy and tissue exposure to contextualize ketamine effects. We report a robust inverse relationship between PLF and NMDA occupancy 7 min after dosing. Moreover, ketamine could produce inhibition or disinhibition of the 40 Hz response in a temporally dynamic manner. These results provide for the first time empirical data to understand how cortical NMDA transmission deficit may lead to opposite modulation of the auditory steady-state response (ASSR). Importantly, our findings posit that 40 Hz ASSR is a pharmacodynamic biomarker for cortical NMDA function that is also robustly translatable. Besides schizophrenia, such a functional biomarker may be of value to neuropsychiatric disorders like bipolar and autism spectrum where 40 Hz ASSR deficits have been documented.
| S-EPMC4946051 | biostudies-literature
Project description:The effects of transcranial direct current stimulation (tDCS) likely depend on cortical N-methyl-D-aspartic acid (NMDA) neurotransmission; however, no previous studies have reported tDCS-mediated modulation of cortical NMDA neurotransmission in humans. The gamma-band auditory steady-state response (ASSR) to a 40 Hz stimulation likely reflects the integrity of cortical NMDA neurotransmission. The present study tested whether the effect of tDCS is reflected in gamma-band ASSRs during a 40 Hz stimulation. Using a double-blind, randomized, crossover study, we performed magnetoencephalography (MEG) and measured the ASSR in 24 healthy participants during 40 Hz of auditory stimulation after prefrontal tDCS (2 mA) or sham (i.e., placebo) treatment. Our results failed to reveal significant differences in any brain between the two conditions after the application of a frequency of approximately 40 Hz. Based on these results, the ASSR is an insufficient method to detect the effect of tDCS on cortical NMDA neurotransmission. Unexpectedly, the results revealed an enhanced beta-band event-related spectral perturbation (ERSP) in the left motor cortex after tDCS compared with that observed after the sham stimuli. Given that beta-band oscillations reflect many functions in motor cortices, the tDCS for the frontal areas had some effect on the left motor cortex while the participants were focusing on not pressing the button with their right index finger. An additional study with an adequate psychological task is necessary to draw a conclusion regarding this unexpected result.
| S-EPMC5830999 | biostudies-literature
Project description:BACKGROUND:Auditory steady state responses (ASSRs) are elicited by clicktrains or amplitude-modulated tones, which entrain auditory cortex at their specific modulation rate. Previous research has reported reductions in ASSRs at 40?Hz for autism spectrum disorder (ASD) participants and first-degree relatives of people diagnosed with ASD (Mol Autism. 2011;2:11, Biol Psychiatry. 2007;62:192-197). METHODS:Using a 1.5?s-long auditory clicktrain stimulus, designed to elicit an ASSR at 40?Hz, this study attempted to replicate and extend these findings. Magnetencephalography (MEG) data were collected from 18 adolescent ASD participants and 18 typically developing controls. RESULTS:The ASSR localised to bilateral primary auditory regions. Regions of interest were thus defined in left and right primary auditory cortex (A1). While the transient gamma-band response (tGBR) from 0-0.1?s following presentation of the clicktrain stimulus was not different between groups, for either left or right A1, the ASD group had reduced oscillatory power at 40?Hz from 0.5 to 1.5?s post-stimulus onset, for both left and right A1. Additionally, the ASD group had reduced inter-trial coherence (phase consistency over trials) at 40?Hz from 0.64-0.82?s for right A1 and 1.04-1.22?s for left A1. LIMITATIONS:In this study, we did not conduct a clinical autism assessment (e.g. the ADOS), and therefore, it remains unclear whether ASSR power and/or ITC are associated with the clinical symptoms of ASD. CONCLUSION:Overall, our results support a specific reduction in ASSR oscillatory power and inter-trial coherence in ASD, rather than a generalised deficit in gamma-band responses. We argue that this could reflect a developmentally relevant reduction in non-linear neural processing.
| S-EPMC7329477 | biostudies-literature