Neuroscience Letters

Neural activity in the olfactory bulb is reflected in local field potentials (LFPs). Functionally, LFPs in the olfactory bulb are categorized into different frequency bands: 1-4 Hz, 6-12 Hz, 25-50 Hz, and 65-130 Hz, which respectively correspond to respiration, sniffing, slow gamma, and fast gamma oscillations. While gamma oscillations in the olfactory bulb are modulated by respiration and sniffing, it remains unknown how and whether the modulation of LFP oscillations is affected by the time of day. To address this question, we recorded LFPs in the olfactory bulb, hippocampus, and neocortex of unrestrained mice for up to 3 d. For each recording site, we calculated the correlation coefficients of normalized LFP powers between pairs of frequency bands in the three regions during the dark and light periods. We then compared these correlations with those generated by surrogate data to investigate whether the correlation was statistically significant. We found that the correlation between sniffing and slow gamma oscillations was higher in the dark period than in the light period. Our finding has the potential to shed light on the coding scheme of olfactory information that is dependent on the light/dark cycle.

Inhibitor-2 (I-2) is a prototypic inhibitor of protein phosphatase-1 (PP1), a major serine-threonine phosphatase that regulates synaptic plasticity and learning and memory. Although I-2 is a potent inhibitor of PP1 in vitro, our previous work has elucidated that, in vivo, I-2 may act as a positive regulator of PP1. Here we show that I-2 and PP1{gamma}, but not PP1, positively regulate synaptic transmission in hippocampal neurons. Moreover, we demonstrated that I-2 enhances PP1{gamma} interaction with its major synaptic scaffold, neurabin, by Forster resonance energy transfer (FRET)/Fluorescence lifetime imaging microscopy (FLIM) studies, while having a limited effect on PP1 autoinhibitory phosphorylation. Furthermore, our study indicates that the effect of I-2 on PP1 activity in vivo is dictated by I-2 threonine-72 phosphorylation. Our work thus demonstrates a molecular mechanism by which I-2 positively regulates PP1 function in synaptic transmission.

Oscillations in the alpha range (8-15 Hz) have been found to appear prominently in the EEG signal when people are awake with their eyes closed, and since their discovery have been considered a fundamental cerebral rhythm. While the mechanism of this oscillation continues to be debated, it has been shown to bear positive relation to memory capacity, attention and a host of other cognitive outcomes. Here we show that this feature is largely undetected in the EEG of adults without post-primary education and access to modern technologies. Furthermore, we show that the spatial extent and energy of the oscillation have wide variation, with energy ranging over a thousand fold across the breath of humanity with no centralizing mean. This represents a divergence in a fundamental functional characteristic of an organ demonstrating both that modernization has had a profound influence on brain dynamics and that a meaningful average human brain does not exist in a dynamical sense.

Exosomes are secreted by every cell in our body under both physiological and pathological conditions. They travel in the blood, CSF, and all studied biofluids. Their biological roles have been reported to include delivery of important physiological cargo between organs and cells, clearance of toxic proteins; maintenance of cellular stasis, and the propagation of disease pathology. In the case of Alzheimers disease (AD) exosomes have been shown to carry pathological proteins such as amyloid, yet the specificity of this association of amyloid and exosomes is unclear. To address this deficiency, we utilized Isothermal Titration Calorimetry (ITC) to measure the binding of amyloid to exosomes. Here we report that A{beta}40 and A{beta}42 bind to exosomes in a saturable and endothermic manner, a phenomenon not observed with the scrambled versions of either peptide. This points to this interaction being more specific than previously understood, and to amyloid associated with exosomes as an important pool of this peptide in the plasma.

BackgroundFragile X syndrome (FXS) is the leading monogenic cause of Autism. No broadly effective support option currently exists for FXS, and drug development has suffered many failures in clinical trials based on promising preclinical findings. Thus, effective translational biomarkers of treatment outcomes are needed. Recently, electroencephalography (EEG) has been proposed as a translational biomarker in FXS. Recent years have seen an exciting emergence of novel EEG signal analyses from FXS patients. However, there is a notable gap in corresponding analyses conducted on animal models of the disorder. Being X-linked, FXS is more prevalent in males than females, and there exist significant phenotype differences between males and females with FXS. Recent studies involving male FXS participants and rodent models have identified an increase in absolute gamma EEG power, while alpha power is found to be either decreased or unchanged. However, there is not enough research on female FXS patients or models. In addition, studying EEG activity in both young and adult FXS patients or rodent models is crucial for better understanding of the disorders effects on brain development. Therefore, using the well established fmr1 knockout (KO) mouse model of FXS, we aim to compare EEG signal between female wild-type (WT) and female model mice at both juvenile and adult ages. MethodsFrontal-parietal differential EEG was recorded using a stand-alone Open-Source Electrophysiology Recording system for Rodents (OSERR). EEG activity was recorded in three different conditions: a) in the subjects home cage, and in the arenas for b) light -dark test and c) open field test. Absolute and relative EEG power as well as peak alpha frequency, theta-beta ratio, phase-amplitude and amplitude-amplitude coupling, and EEG signal complexity were computed for each condition. ResultsIn our study, we found absolute alpha, beta, gamma and total EEG power is increased in the female model compared to WT controls at the juvenile and adult ages. Alongside, relative theta power is decreased in the model. Additionally, phase-amplitude and amplitude-amplitude coupling is altered in the model. Furthermore, peak alpha frequency is increase, and theta-beta ratio is decreased in the model. Lastly, no change in EEG signal complexity is found. Discussion and ConclusionConsistent with most findings from FXS patients and rodent models, our results demonstrated an increase in gamma power in fmr1KO female mice, reinforcing gamma power as a robust and reliable EEG phenotype across FXS models. Additionally, theta-gamma cross frequency amplitude coupling is inversely coupled in female FXS model, which is similar to what has been reported in FXS patients. Overall, our findings reveal that not all EEG biomarkers observed in FXS patients are replicated in the female FXS model. For example, peak alpha frequency, theta-beta ratio, and brain signal complexity showed discrepancies between the mouse models and FXS patients. Additionally, when compared to previously reported EEG changes in male FXS mouse models, our results highlight the presence of a potential sex-based difference in EEG phenotypes at both juvenile and adult stages of fmr1 KO mouse models. Together, our study indicates that certain EEG parameters may be more translatable between rodent models and FXS patients than others and underscore the importance of considering sex and developmental stage as a critical factor when using EEG as a biomarker in FXS research.

Attention control can be achieved in two ways, stimulus-driven bottom-up attention and goal-driven top-down attention. Different visual search tasks involve different attention control. The pop-out task requires more bottom-up attention, whereas the search task involves more top-down attention. P300 which is the positive potential generated by the brain in the latency of 300-600 ms after the stimulus, reflects the processing of cognitive process and is an important component in visual attention. The P300 source is not consistent in the previous researches, our aim therefore, is to study the source location of P300 component based on visual search attention process. Here we use pop-out and search paradigm to get the ERP data of 13 subjects and the fMRI data of 25 subjects, and analyze the source location of P300 using the ERP-fMRI integration technology with high temporal resolution and high spatial resolution. The target differs from the distractor in color and orientation in the pop-out task, whereas the target and the distractor have different orientation and the same color in the search task. ERP results indicate that pop-out induces larger P300 concentrated in the parietal lobe, whereas search induced P300 is more distributed in the frontal lobe. Further ERP and fMRI integration analyses reveal that the left angular gyrus, right postcentral gyrus of parietal lobe and the left superior frontal gyrus (medial orbital) are the source of P300. Our study suggests the contribution of the frontal and parietal lobes to the P300 component.

Depression of sensory input during voluntary muscle contractions has been demonstrated using electrophysiological methods in both animals and humans. However, the association between electrophysiological responses of the sensory system and subjective peripheral sensation (SPS) during a voluntary muscle contraction remains unclear. Our aim in this study was to describe the changes in SPS, spinal -motoneuron excitability (F-wave to M-wave amplitude), and somatosensory evoked potentials (SEPs) during a unilateral pinch-grip task. Outcome variables were measured on the side ipsilateral and contralateral to the muscle contraction, and at rest (control). Participants were 8 healthy men, 20.9{+/-}0.8 years of age. The isometric pinch-grip task was performed at 30% of the maximum voluntary isometric force measured for the right and left hand separately. The appearance rate of the F-wave during the task was significantly higher for the ipsilateral (right) hand than for the contralateral (left) hand and control condition. Although there was no difference in F-wave latency between hands and the control condition, the amplitude of the F-wave was significantly higher for the ipsilateral (right) hand than for the contralateral (left) hand and the control condition. There was no difference in the amplitude of the SEP at N20. However, the amplitude at P25 was significantly lower for the ipsilateral (right) hand than for the contralateral (left) hand and the control condition. The accuracy rate of detecting tactile stimulation, evaluated for 20 repetitions using a Semmes-Weinstein monofilament at the sensory threshold for each participant, was significantly lower during the pinch-grip task for both the ipsilateral (right) and contralateral (left) hand compared to the control condition. Overall, our findings show that SPS and neurophysiological parameters were not modulated in parallel during the task, with changes in subjective sensation preceding changes in electrophysiological indices during the motor task. Our findings provide basic information on sensory-motor coordination.

The specific oscillatory dynamics of intermuscular coupling involved in swallowing, mastication, speech production, and respiration have not been elucidated. This study aimed to explore intermuscular coupling between the tongue and palate that underlies oral functions by analyzing the event-related coherence (ERC) of electromyography (EMG) signals before swallowing, mastication, and speech production. Twenty-two healthy participants performed three oral tasks: swallowing, speech production, and mastication. Sixteen of these participants also completed a combined task involving swallowing immediately after speech. EMG signals were recorded from the tongue and palate, and ERC between tongue and palate EMG was analyzed. Peak ERC was compared across tasks for alpha (8-14 Hz), beta (16-30 Hz), and gamma (32-46 Hz) frequency bands. In all participants, ERC showed significant peaks in all frequency bands before the onset of swallowing, mastication, and speech. Only the ERC values in the beta band were significantly larger for swallowing than for mastication, but not for speech. Moreover, the ERC values for the combined task of swallowing after speech production were significantly smaller than those for the simple swallowing task in the alpha, beta, and gamma bands. The intermuscular oscillatory regulation is more critical for swallowing than for mastication.

There are significant intra-individual and inter-individual variabilities in audiovisual temporal perception. Previous studies have shown that prestimulus neural variability could reflect behavioral variabilities. We aimed to investigate whether prestimulus neural variability can predict behavioral variability in audiovisual temporal perception. Furthermore, We also explored whether prestimulus neural variability directly influences behavioral responses or indirectly impacts perceptual decisions through post-stimulus-evoked responses. We analyzed the electroencephalography (EEG) data from a paradigm where the twenty-eight human subjects performed a simultaneity judgment (SJ) task in the beep-flash stimulus. The prestimulus weighted permutation entropy (WPE) was the indicator of neural variability in this study. We found that prestimulus frontal WPE could predict the individuals TBW in auditory- and visual-leading conditions. In addition, increased prestimulus parietal WPE was associated with more asynchronous responses. Prestimulus frontal WPE may be associated with top-down cognitive control, while parietal WPE may be related to bottom-up cortical excitability. Furthermore, poststimulus evoked responses could mediate the relation between prestimulus WPE and the individuals TBW or perceptual responses. These results suggested that prestimulus WPE was a marker in reflecting intra-individual and inter-individual variabilities in audiovisual temporal perception. Significantly, prestimulus WPE might influence perceptual responses by affecting poststimulus sensory representations.

Recent studies have indicated that the Rho GTPase family and Rho-kinases are associated with psychiatric diseases, such as schizophrenia. Rho-kinases have two subtypes, Rho-kinases 1 and 2 that regulate actin dynamics and mediate neurite outgrowth, spine morphology in neurons, and neurotransmitter release in vitro and ex vivo. However, the precise role of Rho-kinases in neurotransmitter release in vivo remains unclear. To clarify the role of Rho-kinases 1 and 2 in serotonin and dopamine release in the nucleus accumbens (NAc) of mice in vivo, we investigated the effect of a nonselective Rho-kinase inhibitor, fasudil, and a selective Rho-kinase 2 inhibitor, KD025, using an in vivo microdialysis technique. Fasudil perfusion (1-20 M) into the NAc increased the basal extracellular serotonin level but did not affect dopamine levels, whereas KD025 (10-20 M) had little effect on basal serotonin and dopamine levels. Notably, fasudil perfusion into the NAc suppressed depolarization-induced serotonin and dopamine release in a dose-dependent manner, whereas KD025 selectively suppressed depolarization-induced serotonin release. Our results suggested that Rho-kinases 1 and 2 are associated with dopamine and serotonin release, respectively, and that both may have significant but distinct roles in the regulation of serotonin and dopamine release in the NAc.

Abnormalities in dopamine function might be related to psychiatric disorders such as schizophrenia. Even at the same concentration, dopamine exerts opposite effects on information processing in the prefrontal cortex depending on independent dopamine release modes known as tonic and phasic releases. This duality of dopamine prevents a blanket interpretation of the implications of dopamine abnormalities for diseases on the basis of absolute dopamine levels. Moreover, the mechanisms underlying the mode-specific dopamine abnormalities are not clearly understood. Here, we demonstrate that the two modes of dopamine release in the prefrontal cortex of a schizophrenia-like model are disrupted by different mechanisms. In the schizophrenia-like model established by perinatal exposure to inflammatory cytokine, epidermal growth factor, tonic release was enhanced and phasic release was decreased in the prefrontal cortex. We examined the activity of dopamine neurons in the ventral tegmental area (VTA), which sends dopamine projections to the prefrontal cortex, under anesthesia. The activation of VTA dopamine neurons during excitatory stimulation (local application of glutamate or NMDA), which is associated with phasic activity, was blunt in this model. Dopaminergic neuronal activity in the resting state related to tonic release was increased by disinhibition of the dopamine neurons due to the impairment of 5HT2 (5HT2A) receptor-regulated GABAergic inputs. Moreover, chronic administration of risperidone ameliorated this disinhibition of dopaminergic neurons. These results provide an idea about the mechanism of dopamine disturbance in schizophrenia and may be informative in explaining the effects of atypical antipsychotics as distinct from those of typical drugs. SignificanceI discovered that the hypo-NMDA function occurs in midbrain dopaminergic neurons of a schizophrenia-like model instead of the cerebral cortex, which has been the focus of attention so far. This suggests that the schizophrenia glutamate hypothesis may interact with the dopamine hypothesis. Furthermore, it was elucidated that a subpopulation of dorsal raphe serotonergic neurons inhibits VTA dopaminergic neurons in the resting state, resulting in promotion of social behavior. 5HT2 receptor-mediated regulation of inhibitory inputs to the dopaminergic neurons underlies this serotonergic regulation. In the schizophrenia-like model, this regulation by 5HT2 receptors is impaired. Chronic administration of an atypical antipsychotic ameliorates this abnormality. Therefore, this result may represent a mechanism underlying the differential efficacy between atypical and typical antipsychotics.

Although numerous epilepsy-related genes have been identified by unbiased genome-wide screening based on samples from both animal models and patients, the druggable targets for temporal lobe epilepsy (TLE) are still limited. Meanwhile, a large number of candidate genes that might promote or inhibit seizure activities are waiting for further validation. In this study, we first analyzed two public databases and determined the significant down-regulations of two M-type potassium channel genes (KCNQ2/3) expressions in hippocampus samples from TLE patients. Then we reproduced the similar pathological changes in the pilocarpine mouse model of TLE and further detected the decrease of spike frequency adaptation driven by impacted M-currents on dentate gyrus granule neurons. Finally, we employed a small-scale simulation of dentate gyrus network to investigate potential functional consequences of disrupted neuronal excitability. We demonstrated that the impacted spike frequency adaptation of granule cells facilitated the epileptiform activity among the entire network, including prolonged seizure duration and reduced interictal intervals. Our results identify a new mechanism contributing to ictogenesis in TLE and suggest a novel target for the anti-epileptic drug discovery.

Sleep is a fundamental physiological process conserved across most species. As such, deficits in sleep can result in a myriad of psychological and physical health issues. However, the mechanisms underlying the induction of sleep are relatively unknown. Interestingly, general anesthetics cause unconsciousness by positively modulating GABA-A receptors (GABAARs). Based on this observation, it is hypothesized that GABAARs play a critical role in modulating circuits involved in sleep to promote unconsciousness. Recently, the lateral habenula (LHb) has been demonstrated to play a role in sleep physiology and sedation. Specifically, propofol has been shown to excite LHb neurons to promote sedation. However, the mechanism by which this occurs is unknown. Here, we utilize whole-cell voltage and current clamp recordings from LHb neurons obtained from 8-10 week old male mice to determine the physiological mechanisms for this phenomenon. We show that bath application of 1.5M propofol is sufficient to increase LHb neuronal excitability involving synaptic transmission, but not through modulation of intrinsic properties. Additionally, although there is increased LHb neuronal excitability, GABAARs localized postsynaptically on LHb neurons are still responsive to propofol, as indicated by an increase in the decay time. Lastly, we find that propofol increases the synaptic drive onto LHb neurons involving enhanced presynaptic release of both glutamate and GABA. However, the greatest contributor to the potentiated synaptic drive is the increased release of glutamate which shifts the balance of synaptic transmission towards greater excitation. Taken together, this study is the first to identify the physiological basis for why LHb neurons are excited by propofol, rather than inhibited, and as a result promote sedation.

We developed an automated squint assay using both black C57BL/6J and white CD1 mice that measured the interpalpebral fissure area between the upper and lower eyelids as an objective quantification of pain. In C57BL/6J mice, we observed a squint response to increasing doses of a migraine trigger, the neuropeptide CGRP, including a significant response in female mice at a dose below detection by the manual grimace scale. Using the automated software, both C57BL/6J and CD1 mice lacked a detectable photic blink response. The CGRP-related peptide amylin induced squinting behavior in female mice, but not males. These data demonstrate that an automated squint assay can be used as an objective, real-time continuous-scale measure of pain that provides higher precision and real-time analysis compared to manual grimace assessments.

Traditional circadian clock feedback loops include positive branches and negative branches. Per genes belong to the negative branches. There are three subtypes of Per genes named Per1, Per2 and Per3. The relationship among these subtypes has been rarely reported. In this study, we aimed to explore the action between Per1 and Per2 genes, which are known to be critical in the pathogenesis of mood disorder. We revealed that Per1 has a positive action on the expression of Per2, while Per2 shows a negative effect on Per1 expression. This forms a novel feedback loop. Besides, both knockdown and over-expression of Per1 exhibit a pro-depressive effect, indicating a potential mediation in the pathogenesis of major depressive disorder. Correspondingly, knockdown of Per2 induces mania-like behavior, while, over-expression of Per2 produces a pro-depressive effect, suggesting its involvement in the pathophysiology of bipolar disorder. This research may provide an advance in the differential diagnosis between the two diseases in the future. HighlightsO_LIPer1 promotes the expression of Per2, while Per2 inhibit the expression of Per1 in CA1, forming a negative feedback loop. C_LIO_LIBoth knockdown and over-expression of Per1 in CA1 induce depression-like behaviors, while Per2 involves in both mania and depression-like behaviors. C_LI

INTRODUCTIONVentral tegmental area (VTA) dopamine has been implicated in neuropsychiatric symptoms observed in Alzheimers disease (AD) patients. Dopaminergic dysfunction and aberrant firing are observed in mouse AD models, but the specific roles of A{beta} and tau have not been determined. METHODSWe performed electrophysiological recordings of single VTA dopamine neuron firing in the 3xTg-AD model, followed by recordings in amyloid (APPNL-G-F)- and human tau (hTau)-based models to determine the pathological triggers of impaired firing. RESULTSIn vivo dopamine neuron recordings showed fewer spikes in defined bursts in 3xTg-AD mice versus controls. Ex vivo studies showed an impaired ability to sustain firing during depolarization, which was mimicked with depolarized current in wild type neurons. Dopamine neurons transduced with hTau reflected firing aberrations and impaired bursting, but the effects were not recapitulated in the APPNL-G-F model, DISCUSSIONThese results suggest that hTau specifically induces hyperexcitable states within individual dopamine neurons, disrupting burst firing. This dopaminergic dysfunction could compromise reward learning and contribute to the psychiatric symptoms observed in AD.

Speech-evoked brain potentials provide a window into the neural encoding of speech, experience-dependent plasticity, and deficits in central auditory processing from communication disorders. Stronger and faster frequency-following responses (FFRs) and cortical event-related potentials (ERPs) have been interpreted as reflecting more robust and efficient auditory-sensory processing across brainstem and cortical levels. Importantly, these neural signatures relate to real-world listening skills like speech-in-noise (SIN) perception. Yet, how these speech-evoked FFRs/ERPs relate to underlying auditory anatomical structures is unknown. Using a multimodal imaging approach, we recorded FFRs and ERPs to clean and noise-degraded speech sounds to assess the strength of listeners neural encoding of speech at brainstem (FFR) and cortical (ERP) levels. MRI volumetrics of midbrain and transverse temporal gyrus (Heschls gyrus) quantified morphological variation in subcortical and cortical anatomy that underly these EEG potentials. The QuickSIN assessed behavioral SIN abilities. Results showed that larger and thicker right (but not left) Heschls gyrus was related to listeners SIN abilities as well as the size of their cortical ERPs. Structural and functional measures interacted at a subcortical level. For listeners with smaller midbrain volumes, larger speech FFRs were associated with better QuickSIN scores; whereas in individuals with larger midbrain volumes, larger FFRs were related to poorer QuickSIN. Our findings reveal common functional signatures of speech processing (FFRs, ERPs) are constrained by the anatomy of their underlying generators and suggest a complex interplay between auditory brain structure and function in accounting for perceptual SIN capacity.

Psilocybin produces an altered state of consciousness in humans and is associated with complex spatiotemporal changes in brain networks. Given the emphasis on rodent models for mechanistic studies, there is a need for characterization of the effect of psilocybin on brain-wide network dynamics. Previous rodent studies of psychedelics, using electroencephalogram, have primarily been done with sparse electrode arrays that offered limited spatial resolution precluding network level analysis, and have been restricted to lower gamma frequencies. Therefore, in the study, we used electroencephalographic recordings from 27 sites (electrodes) across rat cortex (n=6 male, 6 female) to characterize the effect of psilocybin (0.1 mg/kg, 1 mg/kg, and 10 mg/kg delivered over an hour) on network organization as inferred through changes in node degree (index of network density) and connection strength (weighted phase-lag index). The removal of aperiodic component from the electroencephalogram localized the primary oscillatory changes to theta (4-10 Hz), medium gamma (70-110 Hz), and high gamma (110-150 Hz) bands, which were used for the network analysis. Additionally, we determined the concurrent changes in theta-gamma phase-amplitude coupling. We report that psilocybin, in a dose-dependent manner, 1) disrupted theta-gamma coupling [p<0.05], 2) increased frontal high gamma connectivity [p<0.05] and posterior theta connectivity [p[&le;]0.049], and 3) increased frontal high gamma [p<0.05] and posterior theta [p[&le;]0.046] network density. The medium gamma frontoparietal connectivity showed a nonlinear relationship with psilocybin dose. Our results suggest that high-frequency network organization, decoupled from local theta-phase, may be an important signature of psilocybin-induced non-ordinary state of consciousness.

The predictive processing framework describes perception as a hierarchical predictive model of sensation. Higher-level neural structures constrain the processing at lower-level structures by suppressing synaptic activity induced by predictable sensory input. But when predictions fail, deviant input is forwarded bottom-up as prediction error to update the perceptual model. The earliest prediction error signals identified in the auditory pathway emerge from the nonlemniscal inferior colliculus (IC). The drive that these feedback signals exert on the perceptual model depends on their expected precision, which determines the postsynaptic gain applied in prediction error forwarding. Expected precision is theoretically encoded by the neuromodulatory (e.g., dopaminergic) systems. To test this empirically, we recorded extracellular responses from the rat nonlemniscal IC to oddball and cascade sequences before, during and after the microiontophoretic application of dopamine or eticlopride (a D2-like receptor antagonist). Hence, we studied dopaminergic modulation on the subcortical processing of unpredictable and predictable auditory changes. Results demonstrate that dopamine reduces the net neuronal responsiveness exclusively to unexpected input, without significantly altering the processing of expected auditory events at population level. We propose that, in natural conditions, dopaminergic projections from the thalamic subparafascicular nucleus to the nonlemniscal IC could serve as a precision-weighting mechanism mediated by D2-like receptors. Thereby, the levels of dopamine release in the nonlemniscal IC could modulate the early bottom-up flow of prediction error signals in the auditory system by encoding their expected precision.

Individuals exhibit significant variations in audiovisual temporal order perception. Previous studies have investigated the neural mechanisms underlying these individual differences by analyzing ongoing neural oscillations using stimuli specific to each participant. This study explored whether these effects could extend to different paradigms with the same stimuli across subjects in each paradigm. The two human participants groups performed a temporal order judgment (TOJ) task in two experimental paradigms while recording EEG. One is the beep-flash paradigm, while the other is the stream-bounce paradigm. We focused on the correlation between individual temporal order bias (i.e., point of subjective simultaneity (PSS)) and spontaneous neural oscillations. In addition, we also explored whether the frontal cortex could modulate the correlation through a simple mediation model. We found that the beta band power in the auditory cortex could negatively predict the individuals PSS in the beep-flash paradigm. Similarly, the same effects were observed in the visual cortex during the stream-bounce paradigm. Furthermore, the frontal cortex could influence the power in the sensory cortex and further shape the individuals PSS. These results suggested that the individuals PSS was modulated by auditory or visual cortical excitability depending on the experimental stimuli. The frontal cortex could shape the relation between sensory cortical excitability and the individuals PSS in a top-down manner. In conclusion, our findings indicated that the prefrontal cortex could effectively regulate an individuals temporal order bias, providing insights into audiovisual temporal order perception mechanisms and potential interventions for modulating temporal perception.