Amplitude Of Auditory Evoked Potentials Research Articles

Comparison of evoked potentials across four related developmental encephalopathies

BackgroundDeveloping biomarkers is a priority for drug development for all conditions, but vital in the rare neurodevelopmental disorders where sensitive outcome measures are lacking. We have previously demonstrated the feasibility and tracking of evoked potentials to disease severity in Rett syndrome and CDKL5 deficiency disorder. The aim of the current study is to characterize evoked potentials in two related developmental encephalopathies, MECP2 duplication syndrome and FOXG1 syndrome, and compare across all four groups to better understand the potential of these measures to serve as biomarkers of clinical severity for the developmental encephalopathies.MethodsVisual and auditory evoked potentials were acquired from participants with MECP2 duplication syndrome and FOXG1 syndrome across five sites of the Rett Syndrome and Rett-Related Disorders Natural History Study. A group of age-matched individuals (mean = 7.8 years; range = 1–17) with Rett syndrome, CDKL5 deficiency disorder, and typically-developing participants served as a comparison group. The analysis focused on group-level differences as well as associations between the evoked potentials and measures of clinical severity from the Natural History Study.ResultsAs reported previously, group-level comparisons revealed attenuated visual evoked potentials (VEPs) in participants with Rett syndrome (n = 43) and CDKL5 deficiency disorder (n = 16) compared to typically-developing participants. VEP amplitude was also attenuated in participants with MECP2 duplication syndrome (n = 15) compared to the typically-developing group. VEP amplitude correlated with clinical severity for Rett syndrome and FOXG1 syndrome (n = 5). Auditory evoked potential (AEP) amplitude did not differ between groups, but AEP latency was prolonged in individuals with MECP2 duplication syndrome (n = 14) and FOXG1 syndrome (n = 6) compared to individuals with Rett syndrome (n = 51) and CDKL5 deficiency disorder (n = 14). AEP amplitude correlated with severity in Rett syndrome and CDKL5 deficiency disorder. AEP latency correlated with severity in CDKL5 deficiency disorder, MECP2 duplication syndrome, and FOXG1 syndrome.ConclusionsThere are consistent abnormalities in the evoked potentials in four developmental encephalopathies some of which correlate with clinical severity. While there are consistent changes amongst these four disorders, there are also condition specific findings that need to be further refined and validated. Overall, these results provide a foundation for further refinement of these measures for use in future clinical trials for these conditions.

Learning to detect auditory signals in noise: Active top-down selection and stable change in signal representations.

Training can improve detection of auditory signals in noise. This learning could potentially occur through active top-down selection mechanisms or stable changes in signal representations. Here, participants were trained and tested (pretest vs. posttest design) on abilities to detect pure tone signals in noise. Auditory evoked potentials (AEPs) to tones were gathered under dichotic listening conditions where participants attended to nontonal stimuli in the opposite ear. Improvements in detection sensitivity were observable regardless of tested tone frequency. This was true in generalization between 861 Hz and 1058-Hz tones (Experiment 1a), and when testing a frequency range > 1 octave (Experiment 2). Such learning was not apparent without training (Experiment 1b). In contrast to behavior, AEP amplitude increases from pre- to posttest were partially specific to trained tone frequencies, even when selective attention was diverted to the opposite ear of tone presentation. Placed in the context of previous work, results suggest that changes in active top-down selection mechanisms and stable signal representations both play a role in auditory detection learning. The mismatch between AEP and behavioral effects suggests a need to consider how these different learning processes can impact detection performance in the variety of listening scenarios a listener may face. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Patološki nalaz slušnih evociranih potencijala kod pacijenata sa hipoplazijom vertebralne arterije udruženom sa moždanim udarom posteriorne cirkulacije

The aim of the paper was to determine clinical significance of pathological finding and characteristics of auditory evoked potentials (AEP) in patients with posterior circulation stroke caused by vertebral artery hypoplasia (VAH). The study enrolled 71 patients, 31 of them had posterior circulation stroke. The results of the examinations showed that pathological AEP finding was statistically significantly correlated with posterior circulation stroke (PCS) finding. Changes in AEP amplitude presented a prominent feature of stroke caused by vertebral artery hypoplasia and require further clinical investigations.

Multisite Study of Evoked Potentials in Rett Syndrome.

The aim of the current study was to evaluate the utility of evoked potentials as a biomarker of cortical function in Rett syndrome (RTT). As a number of disease-modifying therapeutics are currently under development, there is a pressing need for biomarkers to objectively and precisely assess the effectiveness of these treatments. Yearly visual evoked potentials (VEPs) and auditory evoked potentials (AEPs) were acquired from individuals with RTT, aged 2 to 37 years, and control participants across 5 sites as part of the Rett Syndrome and Related Disorders Natural History Study. Baseline and year 1 data, when available, were analyzed and the repeatability of the results was tested. Two syndrome-specific measures from the Natural History Study were used for evaluating the clinical relevance of the VEP and AEP parameters. At the baseline study, group level comparisons revealed reduced VEP and AEP amplitude in RTT compared to control participants. Further analyses within the RTT group indicated that this reduction was associated with RTT-related symptoms, with greater severity associated with lower VEP and AEP amplitude. In participants with RTT, VEP and AEP amplitude was also negatively associated with age. Year 1 follow-up data analyses yielded similar findings and evidence of repeatability of EPs at the individual level. The present findings indicate the promise of evoked potentials (EPs) as an objective measure of disease severity in individuals with RTT. Our multisite approach demonstrates potential research and clinical applications to provide unbiased assessment of disease staging, prognosis, and response to therapy. ANN NEUROL 2021;89:790-802.

Stability of Early Auditory Evoked Potential Components Over Extended Test-Retest Intervals in Young Adults.

Synaptic damage from noise exposures can occur even in the absence of changes in hearing sensitivity in animal models. There is an unmet clinical need for measurements sensitive to such damage to the human auditory system that can augment the pure-tone audiogram. Early components (i.e., <10 msec) of the auditory evoked potential (AEP) may be useful noninvasive indicators of synaptic integrity. Wave I is a measure of synchronous neural activity at the level of the synapse between cochlear inner hair cells and the auditory nerve and may be of particular clinical utility. This amplitude measure has historically been classified as too variable in humans to be used for clinical waveform interpretation, though several recent reliability studies have challenged this view. The focus of the present study is to examine across-session stability of early AEP amplitude measures. In this study, amplitudes of early components (wave I, wave V, summating potential [SP]) of the AEP were measured in a cohort of 38 young adults aged 19 to 33 years (21 female). Stability of these amplitude measures was examined in a subset of 12 young adults (8 female), at time intervals ranging from 15 hr to 328 days between tests. Eligibility criteria included normal pure-tone hearing sensitivity, normal tympanometry, and intact acoustic reflexes. Participants were tested at up to four time points. Each evaluation included pure-tone thresholds, tympanometry, speech-in-noise testing, distortion-product otoacoustic emissions (DPOAE), and early AEPs. AEPs were collected in response to click and tone burst stimuli, with both ear canal and mastoid electrode montages. No clinical changes in pure-tone hearing were found between baseline and follow-up visits. Intraclass correlation coefficients (ICCs) indicated good to excellent reliability for wave I and wave V peak-to-trough amplitudes within individuals across time, with greatest reliability (0.92, 95% confidence interval [0.81 to 0.96]) and largest amplitudes for wave I when measured from the ear canal in response to a click stimulus. Other measures such as amplitude ratios of waves V/I and the SP and action potential (AP) showed lower ICC values when measured from the ear canal, with SP/AP ratio demonstrating the lowest reliability. The results of this study suggest that, when recorded under certain conditions, wave I amplitude can be a stable measure in humans. These findings are consistent with previous work and may inform the development of clinical protocols that utilize wave I amplitude to infer inner ear integrity.

Vagus nerve stimulation (VNS)-induced layer-specific modulation of evoked responses in the sensory cortex of rats

Neuromodulation achieved by vagus nerve stimulation (VNS) induces various neuropsychiatric effects whose underlying mechanisms of action remain poorly understood. Innervation of neuromodulators and a microcircuit structure in the cerebral cortex informed the hypothesis that VNS exerts layer-specific modulation in the sensory cortex and alters the balance between feedforward and feedback pathways. To test this hypothesis, we characterized laminar profiles of auditory-evoked potentials (AEPs) in the primary auditory cortex (A1) of anesthetized rats with an array of microelectrodes and investigated the effects of VNS on AEPs and stimulus specific adaptation (SSA). VNS predominantly increased the amplitudes of AEPs in superficial layers, but this effect diminished with depth. In addition, VNS exerted a stronger modulation of the neural responses to repeated stimuli than to deviant stimuli, resulting in decreased SSA across all layers of the A1. These results may provide new insights that the VNS-induced neuropsychiatric effects may be attributable to a sensory gain mechanism: VNS strengthens the ascending input in the sensory cortex and creates an imbalance in the strength of activities between superficial and deep cortical layers, where the feedfoward and feedback pathways predominantly originate, respectively.

Auditory evoked potentials might have the potential to serve as early indicators related to amyloid beta peptide toxicity

PurposeAccumulation of amyloid beta (Aβ) is thought to be the major cause of the development and progression of Alzheimer's disease (AD). The aim of this study is to elucidate the effects of Aβ1-42 at increasing concentrations on auditory evoked potentials (AEPs) and to determine possible changes relevant to the accumulation of Aβ1-42. Materials and methodsIn this study, rats were randomized to following groups (n = 10 per group): sham (0.9% NaCl), Aβ-1 (1 μg/μl), Aβ-2 (2 μg/μl), Aβ-3 (3 μg/μl), Aβ-4 (4 μg/μl), Aβ-5 (6 μg/μl), Aβ-6 (8 μg/μl) and Aβ-7 (10 μg/μl) groups obtained by injection of 5 μl per ventricle. Then, AEPs were recorded in freely-moving rats. Latencies and amplitudes of AEPs, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were obtained in response to auditory stimulus. Furthermore, Aβ1-42 levels were determined in the temporal cortex. ResultsAβ1-42 levels were significantly higher in the temporal cortex in Aβ groups compared to the sham. In frontal and parietal regions, P1N1 amplitudes were significantly decreased in Aβ-3, 4, 5 and 6 groups, and N1P2 amplitudes were significantly decreased in all Aβ groups, whereas in temporal regions, P1N1 and N1P2 amplitudes were decreased in Aβ-2,3,4,5,6 and 7 compared to the sham. In the evoked gamma power and phase synchronization of gamma responses, we detected significant decrease after Aβ-4 group, whereas a significant decrease in the filtered gamma responses was observed in Aβ groups compared to the sham. ConclusionsAEPs might be used as a biomarker to determine the Aβ1-42 related neuronal degeneration in the auditory networks.

Auditory evoked potentials of the plainfin midshipman fish (Porichthys notatus): implications for directional hearing.

The plainfin midshipman (Porichthys notatus) is an acoustically communicative teleost fish. Here, we evaluated auditory evoked potentials (AEPs) in reproductive female midshipman exposed to tones at or near dominant frequencies of the male midshipman advertisement call. An initial series of experiments characterized AEPs at behaviorally relevant suprathreshold sound levels (130-140 dB SPL re. 1 µPa). AEPs decreased in magnitude with increasing stimulus frequency and featured a stereotyped component at twice the stimulus frequency. Recording electrode position was varied systematically and found to affect AEP magnitude and phase characteristics. Later experiments employed stimuli of a single frequency to evaluate contributions of the saccule to the AEP, with particular attention to the effects of sound source azimuth on AEP amplitude. Unilateral excision of saccular otoliths (sagittae) decreased AEP amplitude; unexpectedly, decreases differed for right versus left otolith excision. A final set of experiments manipulated the sound pressure-responsive swim bladder. Swim bladder excision further reduced the magnitude of AEP responses, effectively eliminating responses at the standard test intensity (130 dB SPL) in some animals. Higher-intensity stimulation yielded response minima at forward azimuths ipsilateral to the excised sagitta, but average cross-azimuth modulation generally remained slight. Collectively, the data underscore that electrode position is an essential variable to control in fish AEP studies and suggest that in female midshipman: (1) the saccule contributes to the AEP, but its directionality as indexed by the AEP is limited, (2) a left-right auditory asymmetry may exist and (3) the swim bladder provides gain in auditory sensitivity that may be important for advertisement call detection and phonotaxis.

Acoustic Stimulation Following Sleep Spindle Activity May Enhance Procedural Memory Consolidation During a Nap

Acoustic and electrical brain stimulations are techniques well known to enhance memory consolidation by driving slow oscillations (SO, < 1Hz) and sleep spindle activity. Recent studies have suggested that the temporal relationship between SO and sleep spindle activity may be an important key to understanding memory consolidation mechanisms. We hypothesized that evoking SO after sleep spindle activity may enhance memory consolidation. To derive these spindle-SO pairs, we delivered acoustic stimulation after sleep spindle detection and investigated its effects on memory consolidation with behavioral tests and analyses of neurophysiological features. Thirteen healthy male subjects (mean ± SD age: 26.3 ± 2.4 years) participated in this study. Subjects took a nap with acoustic stimulation after spindle activity detection and a sham nap without acoustic stimulation. All subjects performed word-pair memorization and finger tapping tasks before and after their nap. We found phase-locked SO and delta (1–4 Hz) activity during the stimulation nap in response to acoustic stimuli, and the subjects had a greater improvement in finger tapping tasks after the stimulation nap than after the sham nap (p = 0.014). We found strong motor-learning enhancement after the stimulation nap, but this effect was limited to the subjects who did not demonstrate evoked spindle activity after their acoustic stimulation. Evoked spindle activity occurred in the up-state following the negative peak in auditory evoked potential (AEP), and this activity was observed only in subjects who had a greater AEP amplitude than normal SO. Based on these results, we suggest that subject-specific stimulation parameters, such as acoustic amplitude and timing, improve motor learning, and are appropriate to drive SO without causing a spindle response.

No Effect of Transcranial Direct Current Stimulation of the Auditory Cortex on Auditory-Evoked Potentials.

Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique to change cortical excitability. Its effects are shown for cognitive processing, and behavior in the motor and perceptual domains. However, evidence of tDCS effects in the perceptual domain particularly for auditory processing is rare. Therefore, and in the context of disturbances in auditory processing in psychiatric populations, e.g., in patients with auditory verbal hallucinations, we aimed to investigate the potential modulatory effect of tDCS on the excitability of left posterior temporal cortex in detail. We included 24 healthy participants in a crossover design, applying sham and anodal stimulation in two measurement sessions 1 week apart. Electroencephalography (EEG) was recorded while participants listened to tones before, during, and after stimulation. Amplitudes and latencies of P50, N100, and P200 auditory-evoked potentials (AEP) were compared between anodal and sham stimulation, and between time points before, during, and after tDCS. In contrast to previous studies, results demonstrate no significant differences between stimulation types or time points for any of the investigated AEP amplitudes or latencies. Furthermore, a topographical analysis did not show any topographical differences during peak time periods of the investigated AEP for stimulation types and time points besides a habituation effect. Thus, our results suggest that tDCS modulation of excitability of the left posterior temporal cortex, targeting the auditory cortex, does not have any effect on AEP. This is particularly interesting in the context of tDCS as a potential treatment for changed electrophysiological parameters and symptoms of psychiatric diseases, e.g., lower N100 or auditory verbal hallucinations in schizophrenia.

Behavioral and Auditory Electrophysiological Rebound as a Compensatory Response to the Reinforcing Effects of Morphine

Auditory-evoked potentials (AEPs) can be modified by associative learning, where the appearance of learned compensatory responses (CCRs) may result in the emergence of drug withdrawal symptoms and relapse. Although CCRs’ influence on later attentive and cognitive domains has been extensively examined, contextual conditioned tolerance occurring in preattentive mechanisms operating at earlier stages of information processing has remained largely unexplored. To extend our knowledge on this subject, compensatory changes on the motor and emotional aspects of behavior evoked by contextual cues were investigated with an electronic open field in morphine-pretreated rats challenged with two morphine overdoses (40 and 80 mg/kg). CCRs influence on the AEPs recorded in the central nucleus of the inferior colliculus (CIC) was analyzed with the help of a field potential recording device and a two-chamber shuttle box placed inside a Faraday cage system. The emergence of electrophysiological CCRs was analyzed by recording AEP latency and amplitude elicited in the central nucleus of the IC (CIC) with the aid of a field potential recording device and a two-chamber shuttle box placed inside a Faraday cage system. Behavioral analysis indicated that CCRs ensue in non-familiar contexts. Electrophysiological data revealed increases in the amplitude of AEPs evoked in a non-familiar context. Our results indicate that behavioral learning responses emerge following Pavlovian conditioning even with the use of low and regular doses of morphine over a short-term treatment. Changes in the CIC electrophysiology may indicate that the development of drug dependence occurs covertly in the early stages of sensory information processing.

Short-term 2.1 GHz radiofrequency radiation treatment induces significant changes on the auditory evoked potentials in adult rats

Purpose: There is a growing interest in the usage of radiofrequency radiation (RF) as a noninvasive brain stimulation method. Previously reported data demonstrated that RF exposure caused a change in brain oscillations. Therefore, we aimed to investigate effects of RF on brain oscillation by measuring the auditory response of different brain regions in rats.Materials and methods: Rats were randomly divided into three groups (n = 12 per each group): Cage control (C), sham rats (Sh), and rats exposed to 2.1 GHz RF for 2 h/day for 7 days. At the end of the exposure, auditory evoked potentials (AEPs) were recorded at different locations in rats. Latencies and amplitudes of AEPs, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were obtained in response to an auditory stimulus. Furthermore, TBARS levels and 4-HNE, GFAP, iNOS, and nNOS expressions were evaluated in all groups.Results: Peak-to-peak amplitudes of AEPs were significantly higher in the RF group compared with the Sh group. There is no significant difference in peak latencies of AEPs between groups. Beside, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were significantly higher in the RF group compared with the Sh group. In addition, the RF group had significantly lower TBARS and 4-HNE levels than the Sh group. There were no significant differences between groups for GFAP, nNOS, and iNOS levels, and between the C and RF groups for all parameters.Conclusions: Our present findings suggest that short-term RF treatment under chosen experimental conditions have statistically significant effect on neuronal networks of rats by probably reducing oxidative damage. However, this effect must be further studied for possible noninvasive brain stimulation.

Loudness- and time-dependence of auditory evoked potentials is blunted by the NMDA channel blocker MK-801

Amplitudes of auditory evoked potentials (AEP) increase with the intensity/loudness of sounds (loudness-dependence of AEP, LDAEP), and the time between adjacent sounds (time-dependence of AEP, TDAEP). Both, blunted LDAEP and blunted TDAEP are markers of altered auditory function in schizophrenia (SZ). However, while blunted LDAEP has been attributed to altered serotonergic function, blunted TDAEP has been linked to altered NMDA receptor function. Despite phenomenological similarities of the two effects, no common pharmacological underpinnings have been identified. To test whether LDAEP and TDAEP are both affected by NMDA receptor blockade, two rhesus macaques passively listened to auditory clicks of 5 different intensities presented with stimulus-onset asynchronies ranging between 0.2 and 6.4s. 8 AEP components were analyzed, including the N85, the presumed human N1 homolog. LDAEP and TDAEP were estimated as the slopes of AEP amplitude with intensity and the logarithm of stimulus-onset asynchrony, respectively. On different days, AEPs were collected after systemic injection of MK-801 or vehicle. Both TDAEP and LDAEP of the N85 were blunted by the NMDA blocker MK-801 and recapitulate the SZ phenotype. In summary, LDAEP and TDAEP share important pharmacological commonalities that may help identify a common pharmacological intervention to normalize both electrophysiological phenotypes in SZ.

Modulation of mGlu2 Receptors, but Not PDE10A Inhibition Normalizes Pharmacologically-Induced Deviance in Auditory Evoked Potentials and Oscillations in Conscious Rats.

Improvement of cognitive impairments represents a high medical need in the development of new antipsychotics. Aberrant EEG gamma oscillations and reductions in the P1/N1 complex peak amplitude of the auditory evoked potential (AEP) are neurophysiological biomarkers for schizophrenia that indicate disruption in sensory information processing. Inhibition of phosphodiesterase (i.e. PDE10A) and activation of metabotropic glutamate receptor (mGluR2) signaling are believed to provide antipsychotic efficacy in schizophrenia, but it is unclear whether this occurs with cognition-enhancing potential. The present study used the auditory paired click paradigm in passive awake Sprague Dawley rats to 1) model disruption of AEP waveforms and oscillations as observed in schizophrenia by peripheral administration of amphetamine and the N-methyl-D-aspartate (NMDA) antagonist phencyclidine (PCP); 2) confirm the potential of the antipsychotics risperidone and olanzapine to attenuate these disruptions; 3) evaluate the potential of mGluR2 agonist LY404039 and PDE10 inhibitor PQ-10 to improve AEP deficits in both the amphetamine and PCP models. PCP and amphetamine disrupted auditory information processing to the first click, associated with suppression of the P1/N1 complex peak amplitude, and increased cortical gamma oscillations. Risperidone and olanzapine normalized PCP and amphetamine-induced abnormalities in AEP waveforms and aberrant gamma/alpha oscillations, respectively. LY404039 increased P1/N1 complex peak amplitudes and potently attenuated the disruptive effects of both PCP and amphetamine on AEPs amplitudes and oscillations. However, PQ-10 failed to show such effect in either models. These outcomes indicate that modulation of the mGluR2 results in effective restoration of abnormalities in AEP components in two widely used animal models of psychosis, whereas PDE10A inhibition does not.

V34. Paired associative stimulation of the temporal cortex

Background Paired associative stimulation (PAS) is a specific repetitive transcranial magnetic stimulation (rTMS) protocol where every pulse is combined with an external stimulus. Based on a close timing between the TMS induced action potential and the cortical arrival of the external stimulus in the stimulated area neural plasticity is induced by mechanisms of spike-timing dependent plasticity. After a first proof-of-principle study of PAS of the auditory cortex by our group, we here extend these findings by investigating the effects of stimulus duration and of sham stimulation on primary and secondary auditory cortical activity. Methods The left temporal cortex of 18 healthy controls with normal hearing was stimulated in two experimental parts. One PAS session consisted of 200 stimulations with an interstimulus interval of 45 ms between tone onset (400 ms length, 4 kHz frequency) and the TMS pulse proven to be effective in the pilot study. Part 1 contrasted effects of a short (23 ms) and a long (400 ms) PAS-tone on secondary auditory cortex activity (short vs. long condition); part 2 contrasted effects of verum and sham stimulation (6-fold reduced intensity, not targeting the cortex) on primary and secondary auditory cortex activity (verum vs. sham condition). Primary auditory cortex activity was measured with auditory steady state responses (ASSR) as elicited by 40 Hz amplitude-modulated (AM) sine tones. Secondary auditory cortex activity was elicited with ASSRs using a 20 Hz AM tone and late auditory evoked potentials (AEPs) for the 40 Hz and 20 Hz AM tone. Evoked activity was done for the PAS tone (4 kHz carrier frequency) and a control tone (1 kHz carrier frequency) - each tone presented 70 times (60 dB SL, 800 ms length). As STDP is based on close timing of pre- and post-synaptic activity we concentrated on evoked activity by using analyses time-locked to the tone onset. Results For part 1, the short PAS condition showed an increase in AEP amplitude accompanied by a decrease for the long PAS condition specific for the PAS carrier frequency. Verum and sham stimulation showed comparable decreases in AEP amplitude independent from the PAS protocol. Part 2 showed no effects for the contrast short vs. long condition. 20 Hz ASSR amplitude showed sham-controlled decreases for the PAS-specific carrier frequency. ASSR amplitudes of the control tone or of the 40 Hz AM tone showed no significant effects. Discussion PAS of the auditory cortex seem to be restricted to the secondary auditory cortex as effects could only be found for the AEPs and the 20 Hz ASSRs which have neural generators rather in secondary than in primary auditory cortex. AEPs findings raise the importance of habituation effects and of duration of the PAS tone and challenge the validity of the transfer of PAS using sine tones to evoked potentials using AM tones.

Covariation of pupillary and auditory cortical activity in rats under isoflurane anesthesia

Very slow fluctuations of spontaneous activities significantly influence not only behavioral performance in a conscious state, but also neural activities in an unconscious state. Covariation of pupil and cortical activities may lend important insights into the state-dependent modulation of stimulus encoding, yet this phenomenon has received little attention, especially with regard to non-visual cortices. In the present study, we investigated co-fluctuation of pupil size and neural activity in the auditory cortex of rats under isoflurane anesthesia. Pupil fluctuation consisted of longitudinal irregular shifts, and 1-min cyclic modulations. Both spontaneous and auditory-evoked potentials (AEPs) covaried with the longitudinal fluctuation of pupil size, but not with the 1-min cycle. Pupil size exhibited a positive correlation with spontaneous activity and negative correlation with AEP amplitude, particularly when the pupil size was beyond the normal range. Stimulus-specific adaptation characterized using an oddball paradigm was less dependent on pupil size than AEP. In contrast to the cortical activity, heart rate covaried with pupil size with the 1-min oscillatory component, but not the non-oscillatory component. Furthermore, light exposure induced the pupil reflex through the autonomic system, but did not modify cortical activity, indicating that autonomic activity was not causing the cortical modulation. These results together suggest that cortical activities spontaneously covary with pupillary activity through central cholinergic modulation that triggers sympathetic nerve activation. Such a state-dependent property may be a confounding factor in cortical electrophysiology studies.

Histological correlates of N40 auditory evoked potentials in adult rats after neonatal ventral hippocampal lesion: animal model of schizophrenia

The neonatal ventral hippocampal lesion (NVHL) is an established neurodevelopmental rat model of schizophrenia. Rats with NVHL exhibit several behavioral, molecular and physiological abnormalities that are similar to those found in schizophrenics. Schizophrenia is a severe psychiatric illness characterized by profound disturbances of mental functions including neurophysiological deficits in brain information processing. These deficits can be assessed by auditory evoked potentials (AEPs), where schizophrenics exhibit abnormalities in amplitude, duration and latency of such AEPs. The aim of the present study was to compare the density of cells in the temporal cerebral cortex and the N40-AEP of adult NVHL rats versus adult sham rats. We found that rats with NVHL exhibit significant lower amplitude of the N40-AEP and a significant lower number of cells in bilateral regions of the temporal cerebral cortex compared to sham rats. Because the AEP recordings were obtained from anesthetized rats, we suggest that NVHL leads to inappropriate innervation in thalamic-cortical pathways in the adult rat, leading to altered function of cortical networks involved in processing of primary auditory information.

Mechanisms of distance-invariant recognition of target strength in the biosonar of odontocetes

Invariant target recognition by sonar requires assessment of the target strength invariably of distance despite wide variation of the echo level. Information on the echo delay and the level of the emitted pulse allows computing of the target strength. The question is: which particular mechanisms perform this computation in the biosonar of odontocetes? Investigations of the auditory evoked potentials (AEPs) during echolocation in several odontocetes have shown that comparison of the emitted pulse level, echo delay, and echo level is based on the forward masking of the echo-response by the preceding self-heard emitted click. Prolongation of the echo delay results in releasing of the echo-related AEP from masking. This release from masking compensated for the echo attenuation with distance. As a result, the echo-related AEP amplitude depended on the target strength and little depended on the target distance. Moreover, the forward-masking duration depended on the level of the emitted pulse. As a result, the echo-related AEP featured amplitude little depended on the level of the emitted pulse. The constancy of the echo-related AEP amplitude indicates the dependence of sensation level of the echo only on the target strength and the independence of both emitted click level and target distance.

Functional Connectivity from the Amygdala to the Hippocampus Grows Stronger after Stress

The cellular and molecular effects of stress on the amygdala are strikingly different compared with those in the hippocampus. Previous findings on stress-induced plasticity were based primarily on postmortem analysis within individual areas. However, little is known about how stress affects dynamic changes and interactions in neuronal activity between the two areas. Hence, we simultaneously monitored in vivo activity of neuronal populations located in hippocampal areas CA1 and CA3 and the lateral amygdala (LA) in rats during and after chronic immobilization stress. The amplitude of auditory-evoked potentials (AEPs) in the hippocampus increased transiently only after a single 2 h stress but not when it was repeated for 10 d. In contrast, both acute and chronic stress caused a persistent increase in AEPs in the LA. Chronic stress also elicited a sustained increase in the LA but a decrease in the hippocampus in the evoked power of gamma and beta frequencies. Moreover, beta and gamma synchrony was reduced between areas CA1 and CA3 but enhanced between the LA and hippocampus after chronic stress. Granger causality spectra revealed a strong directional influence from the LA to area CA1 that persisted throughout and even 10 d after chronic stress. However, directional coupling from hippocampal area CA3 to CA1 became weaker at the end of chronic stress. Thus, our findings suggest that the growing dominance of amygdalar activity over the hippocampus during and even after chronic stress may contribute to the enhanced emotional symptoms, alongside impaired cognitive function, seen in stress-related psychiatric disorders.

Neurophysiology and Intraoperative Nociception

Neurophysiology and Intraoperative Nociception