The influence of electrode types to the visually induced gamma oscillations in mouse primary visual cortex.

The local field potential (LFP) is an extracellular electrical signal associated with neural ensemble input and dendritic signaling. Previous studies have linked gamma band oscillations of the LFP in cortical circuits to sensory stimuli encoding, attention, memory, and perception. Inconsistent results regarding gamma tuning for visual features were reported, but it remains unclear whether these discrepancies are due to variations in electrode properties. Specifically, the surface area and impedance of the electrode are important characteristics in LFP recording. To comprehensively address these issues, we conducted an electrophysiological study in the V1 region of lightly anesthetized mice using two types of electrodes: one with higher impedance (1 MΩ) and a sharp tip (10 µm), while the other had lower impedance (100 KΩ) but a thicker tip (200 µm). Our findings demonstrate that gamma oscillations acquired by sharp-tip electrodes were significantly stronger than those obtained from thick-tip electrodes. Regarding size tuning, most gamma power exhibited surround suppression at larger gratings when recorded from sharp-tip electrodes. However, the majority showed enhanced gamma power at larger gratings when recorded from thick-tip electrodes. Therefore, our study suggests that microelectrode parameters play a significant role in accurately recording gamma oscillations and responsive tuning to sensory stimuli.

Visually induced γ band rhythm in spatial summation beyond the receptive field in mouse primary visual cortex.

Recent studies in many kinds of mammals have established the existence of multiple γ rhythms in the cerebral cortex subserving different functions. In the primary visual cortex (V1), visually induced γ rhythms are dependent on stimulus features. However, experimental findings of γ power induced by varying the size of the drifting grating are inconsistent. Here, we reinvestigated the spatial summation properties of visually induced spike and γ rhythm activities in mouse V1. Our results show that drifting sinusoidal grating stimuli mainly induce 2 γ band rhythms, including a low-frequency band (25-45 Hz) and a high-frequency band (55-75 Hz). Unlike previous findings, we discovered that visually induced γ power could also exhibit extrareceptive field (ERF) modulatory properties. The modulation by ERF stimulation could be either suppressive, countersuppressive, or nonsuppressive, mostly similar to the local spike activity. Moreover, further analysis of the neuron group exhibiting surround suppression in both spike and γ activity revealed that the strength of the surround suppression and the receptive field size showed moderate correlations between measurements by spike and γ rhythm activity. Our findings improve the understanding of the characteristics and neural mechanisms of induced γ rhythms in visual spatial summation.

Dose-related adaptive reconstruction of DMN in isoflurane administration: a study in the rat.

BACKGROUND: The anesthetic states are accompanied by functional alterations. However, the dose-related adaptive alterations in the higher-order network under anesthesia, e. g. default mode network (DMN), are poorly revealed. METHODS: We implanted electrodes in brain regions of the rat DMN to acquire local field potentials to investigate the perturbations produced by anesthesia. Relative power spectral density, static functional connectivity (FC), fuzzy entropy of dynamic FC, and topological features were computed from the data. RESULTS: The results showed that adaptive reconstruction was induced by isoflurane, exhibiting reduced static and stable long-range FC, and altered topological features. These reconstruction patterns were in a dose-related fashion. CONCLUSION: These results might impart insights into the neural network mechanisms underlying anesthesia and suggest the potential of monitoring the depth of anesthesia based on the parameters of DMN.

Computational exploration of dynamic mechanisms of steady state visual evoked potentials at the whole brain level.

Periodic visual stimulation can induce stable steady-state visual evoked potentials (SSVEPs) distributed in multiple brain regions and has potential applications in both neural engineering and cognitive neuroscience. However, the underlying dynamic mechanisms of SSVEPs at the whole-brain level are still not completely understood. Here, we addressed this issue by simulating the rich dynamics of SSVEPs with a large-scale brain model designed with constraints of neuroimaging data acquired from the human brain. By eliciting activity of the occipital areas using an external periodic stimulus, our model was capable of replicating both the spatial distributions and response features of SSVEPs that were observed in experiments. In particular, we confirmed that alpha-band (8-12 Hz) stimulation could evoke stronger SSVEP responses; this frequency sensitivity was due to nonlinear entrainment and resonance, and could be modulated by endogenous factors in the brain. Interestingly, the stimulus-evoked brain networks also exhibited significant superiority in topological properties near this frequency-sensitivity range, and stronger SSVEP responses were demonstrated to be supported by more efficient functional connectivity at the neural activity level. These findings not only provide insights into the mechanistic understanding of SSVEPs at the whole-brain level but also indicate a bright future for large-scale brain modeling in characterizing the complicated dynamics and functions of the brain.

State-independent and state-dependent patterns in the rat default mode network.

Resting-state studies have typically assumed constant functional connectivity (FC) between brain regions, and these parameters of interest provide meaningful descriptions of the functional organization of the brain. A number of studies have recently provided evidence pointing to dynamic FC fluctuations in the resting brain, especially in higher-order regions such as the default mode network (DMN). The neural activities underlying dynamic FC remain poorly understood. Here, we recorded electrophysiological signals from DMN regions in freely behaving rats. The dynamic FCs between signals within the DMN were estimated by the phase locking value (PLV) method with sliding time windows across vigilance states [quiet wakefulness (QW) and slow-wave and rapid eye movement sleep (SWS and REMS)]. Factor analysis was then performed to reveal the hidden patterns within the DMN. We identified distinct spatial FC patterns according to the similarities between their temporal dynamics. Interestingly, some of these patterns were vigilance state-dependent, while others were independent across states. The temporal contributions of these patterns fluctuated over time, and their interactive relationships were different across vigilance states. These spatial patterns with dynamic temporal contributions and combinations may offer a flexible framework for efficiently integrating information to support cognition and behavior. These findings provide novel insights into the dynamic functional organization of the rat DMN.

Correction: Spatiotemporal network coding of physiological mossy fiber inputs by the cerebellar granular layer.

[This corrects the article DOI: 10.1371/journal.pcbi.1005754.].

Spatiotemporal network coding of physiological mossy fiber inputs by the cerebellar granular layer.

The granular layer, which mainly consists of granule and Golgi cells, is the first stage of the cerebellar cortex and processes spatiotemporal information transmitted by mossy fiber inputs with a wide variety of firing patterns. To study its dynamics at multiple time scales in response to inputs approximating real spatiotemporal patterns, we constructed a large-scale 3D network model of the granular layer. Patterned mossy fiber activity induces rhythmic Golgi cell activity that is synchronized by shared parallel fiber input and by gap junctions. This leads to long distance synchrony of Golgi cells along the transverse axis, powerfully regulating granule cell firing by imposing inhibition during a specific time window. The essential network mechanisms, including tunable Golgi cell oscillations, on-beam inhibition and NMDA receptors causing first winner keeps winning of granule cells, illustrate how fundamental properties of the granule layer operate in tandem to produce (1) well timed and spatially bound output, (2) a wide dynamic range of granule cell firing and (3) transient and coherent gating oscillations. These results substantially enrich our understanding of granule cell layer processing, which seems to promote spatial group selection of granule cell activity as a function of timing of mossy fiber input.

Critical Roles of the Direct GABAergic Pallido-cortical Pathway in Controlling Absence Seizures.

The basal ganglia (BG), serving as an intermediate bridge between the cerebral cortex and thalamus, are believed to play crucial roles in controlling absence seizure activities generated by the pathological corticothalamic system. Inspired by recent experiments, here we systematically investigate the contribution of a novel identified GABAergic pallido-cortical pathway, projecting from the globus pallidus externa (GPe) in the BG to the cerebral cortex, to the control of absence seizures. By computational modelling, we find that both increasing the activation of GPe neurons and enhancing the coupling strength of the inhibitory pallido-cortical pathway can suppress the bilaterally synchronous 2-4 Hz spike and wave discharges (SWDs) during absence seizures. Appropriate tuning of several GPe-related pathways may also trigger the SWD suppression, through modulating the activation level of GPe neurons. Furthermore, we show that the previously discovered bidirectional control of absence seizures due to the competition between other two BG output pathways also exists in our established model. Importantly, such bidirectional control is shaped by the coupling strength of this direct GABAergic pallido-cortical pathway. Our work suggests that the novel identified pallido-cortical pathway has a functional role in controlling absence seizures and the presented results might provide testable hypotheses for future experimental studies.

Bidirectional control of absence seizures by the basal ganglia: a computational evidence.

Absence epilepsy is believed to be associated with the abnormal interactions between the cerebral cortex and thalamus. Besides the direct coupling, anatomical evidence indicates that the cerebral cortex and thalamus also communicate indirectly through an important intermediate bridge-basal ganglia. It has been thus postulated that the basal ganglia might play key roles in the modulation of absence seizures, but the relevant biophysical mechanisms are still not completely established. Using a biophysically based model, we demonstrate here that the typical absence seizure activities can be controlled and modulated by the direct GABAergic projections from the substantia nigra pars reticulata (SNr) to either the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of thalamus, through different biophysical mechanisms. Under certain conditions, these two types of seizure control are observed to coexist in the same network. More importantly, due to the competition between the inhibitory SNr-TRN and SNr-SRN pathways, we find that both decreasing and increasing the activation of SNr neurons from the normal level may considerably suppress the generation of spike-and-slow wave discharges in the coexistence region. Overall, these results highlight the bidirectional functional roles of basal ganglia in controlling and modulating absence seizures, and might provide novel insights into the therapeutic treatments of this brain disorder.

Disruption of TLE epileptiform activity retarded the seizure and reduced pathological HFOs.

In temporal lobe epilepsy (TLE), the epileptogenic zones, such as the temporal lobe structure, could generate pathological high-frequency oscillations (pHFOs, 250-500 Hz) before the ictal period. These pHFOs have also been observed during the process of seizures in both TLE patients and animals, exhibiting a critical role as promising biomarkers for TLE seizures. TLE seizures could be modulated via regulating the neural excitability in epileptogenic zones, for that TLE is primarily associated with the excitation-inhibition imbalance. However, whether these kinds of modulations could also impact the pHFOs characteristics during TLE seizures is still unclear. For this purpose, we pharmaco-genetically inhibited the principal cells (PCs) in the mouse CA3 region and tracked the difference in the behavioral and electrophysiological features during LiCl-pilocarpine-induced TLE seizure between the hM4Di+CNO (experimental) mice and mCherry+CNO (control) mice. Delayed latency, decreased averaged duration, and reduced counts of the generalized seizure were observed in the experimental mice. Besides, the electrophysiological characteristics, such as the firing rate of PCs and the count of pHFO, exhibited significant decline in the CA3 and CA1 regions. During TLE seizure, there existed strong phase-coupling between pHFO and PCs spike timing in the control mice, while it was abolished in the experimental mice. In addition, we also found that the counts of pHFO were significantly associated with the behavioral features, indicating the close relationships within them. Collectively, our findings suggested that alterations in pHFO and the retardation of seizures may be attributed to disruptions in neuronal excitability, and the variations of electrophysiological features were related to seizure severity during TLE seizures. These results provide valuable insights into the role of pHFOs in TLE and shed light on the underlying mechanisms involved.

Reliable object tracking by multimodal hybrid feature extraction and transformer-based fusion.

Visual object tracking, which is primarily based on visible light image sequences, encounters numerous challenges in complicated scenarios, such as low light conditions, high dynamic ranges, and background clutter. To address these challenges, incorporating the advantages of multiple visual modalities is a promising solution for achieving reliable object tracking. However, the existing approaches usually integrate multimodal inputs through adaptive local feature interactions, which cannot leverage the full potential of visual cues, thus resulting in insufficient feature modeling. In this study, we propose a novel multimodal hybrid tracker (MMHT) that utilizes frame-event-based data for reliable single object tracking. The MMHT model employs a hybrid backbone consisting of an artificial neural network (ANN) and a spiking neural network (SNN) to extract dominant features from different visual modalities and then uses a unified encoder to align the features across different domains. Moreover, we propose an enhanced transformer-based module to fuse multimodal features using attention mechanisms. With these methods, the MMHT model can effectively construct a multiscale and multidimensional visual feature space and achieve discriminative feature modeling. Extensive experiments demonstrate that the MMHT model exhibits competitive performance in comparison with that of other state-of-the-art methods. Overall, our results highlight the effectiveness of the MMHT model in terms of addressing the challenges faced in visual object tracking tasks.

A Spatial-Channel-Temporal-Fused Attention for Spiking Neural Networks.

Spiking neural networks (SNNs) mimic brain computational strategies, and exhibit substantial capabilities in spatiotemporal information processing. As an essential factor for human perception, visual attention refers to the dynamic process for selecting salient regions in biological vision systems. Although visual attention mechanisms have achieved great success in computer vision applications, they are rarely introduced into SNNs. Inspired by experimental observations on predictive attentional remapping, we propose a new spatial-channel-temporal-fused attention (SCTFA) module that can guide SNNs to efficiently capture underlying target regions by utilizing accumulated historical spatial-channel information in the present study. Through a systematic evaluation on three event stream datasets (DVS Gesture, SL-Animals-DVS, and MNIST-DVS), we demonstrate that the SNN with the SCTFA module (SCTFA-SNN) not only significantly outperforms the baseline SNN (BL-SNN) and two other SNN models with degenerated attention modules, but also achieves competitive accuracy with the existing state-of-the-art (SOTA) methods. Additionally, our detailed analysis shows that the proposed SCTFA-SNN model has strong robustness to noise and outstanding stability when faced with incomplete data, while maintaining acceptable complexity and efficiency. Overall, these findings indicate that incorporating appropriate cognitive mechanisms of the brain may provide a promising approach to elevate the capabilities of SNNs.

A model description of beta oscillations in the external globus pallidus.

The external globus pallidus (GPe), a subcortical nucleus located in the indirect pathway of the basal ganglia, is widely considered to have tight associations with abnormal beta oscillations (13-30 Hz) observed in Parkinson's disease (PD). Despite that many mechanisms have been put forward to explain the emergence of these beta oscillations, however, it is still unclear the functional contributions of the GPe, especially, whether the GPe itself can generate beta oscillations. To investigate the role played by the GPe in producing beta oscillations, we employ a well described firing rate model of the GPe neural population. Through extensive simulations, we find that the transmission delay within the GPe-GPe pathway contributes significantly to inducing beta oscillations, and the impacts of the time constant and connection strength of the GPe-GPe pathway on generating beta oscillations are non-negligible. Moreover, the GPe firing patterns can be significantly modulated by the time constant and connection strength of the GPe-GPe pathway, as well as the transmission delay within the GPe-GPe pathway. Interestingly, both increasing and decreasing the transmission delay can push the GPe firing pattern from beta oscillations to other firing patterns, including oscillation and non-oscillation firing patterns. These findings suggest that if the transmission delays within the GPe are at least 9.8 ms, beta oscillations can be produced originally in the GPe neural population, which also may be the origin of PD-related beta oscillations and should be regarded as a promising target for treatments for PD.

Differential patterns of very high-frequency oscillations in two seizure types of the pilocarpine-induced TLE model.

AIMS: Very high-frequency oscillations (VHFOs, >500 Hz) are considered a highly sensitive biomarker of seizures. We hypothesized that VHFOs may exhibit specificity towards hypersynchronous (HYP) seizures and low-voltage fast (LVF) seizures in temporal lobe epilepsy (TLE). METHODS: Local field potentials were recorded from the hippocampal network in TLE mice induced by pilocarpine. Subsequently, we analyzed the VHFO features, including their temporal-frequency characteristics and VHFO/theta coupling, during three states: baseline, preictal, and postictal for both HYP- and LVF-seizure groups. RESULTS: Significant changes in most of the VHFO features were observed during the preictal state in both seizure groups. In the postictal state, VHFO features in the HYP-seizure group exhibited inverse alterations and appeared to align with those observed during baseline conditions. However, such phenomena were not observed after TLE seizures in the LVF-seizure group. CONCLUSION: Our findings highlight distinct patterns of VHFO feature changes across different states of HYP seizures and LVF seizures. These results suggest that VHFOs could serve as indicative biomarkers for seizure alterations specifically associated with HYP-seizure states.

Correction to: Bacomics: a comprehensive cross area originating in the studies of various brain-apparatus conversations.

[This corrects the article DOI: 10.1007/s11571-020-09577-7.].

Stochastic resonance in Hodgkin-Huxley neuron induced by unreliable synaptic transmission.

We systematically investigate the stochastic dynamics of a single Hodgkin-Huxley neuron driven by stochastic excitatory and inhibitory input spikes via unreliable synapses in this paper. Based on the mean-filed theory, a novel intrinsic neuronal noise regulation mechanism stemming from unreliable synapses is presented. Our simulation results show that, under certain conditions, the stochastic resonance phenomenon is able to be induced by the unreliable synaptic transmission, which can be well explained by the theoretical prediction. To a certain degree, the results presented here provide insights into the functional roles of unreliable synapses in neural information processing.

HMGB1-RAGE Pathway Contributes to the Abnormal Migration of Endogenous Subventricular Zone Neural Progenitors in an Experimental Model of Focal Microgyria.

Abnormal migration of subventricular zone (SVZ)-derived neural progenitor cells (SDNPs) is involved in the pathological and epileptic processes of focal cortical dysplasias (FCDs), but the underlying mechanisms are not clear. Recent studies indicated that high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) are widely expressed in epileptic specimens of FCDs, which suggests that the HMGB1-RAGE pathway is involved in the pathological and/or epileptic processes of FCDs. The present study used Nestin-GFPtg/+ transgenic mice, and we established a model of freezing lesion (FL), as described in our previous report. A "migrating stream" composed of GFP-Nestin+ SDNPs was derived from the SVZ region and migrated to the cortical FL area. We found that translocated HMGB1 and RAGE were expressed in cortical lesion in a clustered distribution pattern, which was especially obvious in the early stage of FL compared to the sham group. Notably, the number of GFP-Nestin+ SDNPs within the "migrating stream" was significantly decreased when the HMGB1-RAGE pathway was blocked by a RAGE antagonist or deletion of the RAGE gene. The absence of RAGE also decreased the activity of pentylenetetrazol-induced cortical epileptiform discharge. In summary, this study provided experimental evidence that the levels of extranuclear HMGB1 and its receptor RAGE were increased in cortical lesion in the early stage of the FL model. Activation of the HMGB1-RAGE pathway may contribute to the abnormal migration of SDNPs and the hyperexcitability of cortical lesion in the FL model.

Signal propagation in feedforward neuronal networks with unreliable synapses.

In this paper, we systematically investigate both the synfire propagation and firing rate propagation in feedforward neuronal network coupled in an all-to-all fashion. In contrast to most earlier work, where only reliable synaptic connections are considered, we mainly examine the effects of unreliable synapses on both types of neural activity propagation in this work. We first study networks composed of purely excitatory neurons. Our results show that both the successful transmission probability and excitatory synaptic strength largely influence the propagation of these two types of neural activities, and better tuning of these synaptic parameters makes the considered network support stable signal propagation. It is also found that noise has significant but different impacts on these two types of propagation. The additive Gaussian white noise has the tendency to reduce the precision of the synfire activity, whereas noise with appropriate intensity can enhance the performance of firing rate propagation. Further simulations indicate that the propagation dynamics of the considered neuronal network is not simply determined by the average amount of received neurotransmitter for each neuron in a time instant, but also largely influenced by the stochastic effect of neurotransmitter release. Second, we compare our results with those obtained in corresponding feedforward neuronal networks connected with reliable synapses but in a random coupling fashion. We confirm that some differences can be observed in these two different feedforward neuronal network models. Finally, we study the signal propagation in feedforward neuronal networks consisting of both excitatory and inhibitory neurons, and demonstrate that inhibition also plays an important role in signal propagation in the considered networks.

Induction and propagation of transient synchronous activity in neural networks endowed with short-term plasticity.

Transient, task related synchronous activity within neural populations has been recognized as the substrate of temporal coding in the brain. The mechanisms underlying inducing and propagation of transient synchronous activity are still unknown, and we propose that short-term plasticity (STP) of neural circuits may serve as a supplemental mechanism therein. By computational modeling, we showed that short-term facilitation greatly increases the reactivation rate of population spikes and decreases the latency of response to reactivation stimuli in local recurrent neural networks. Meanwhile, the timing of population spike reactivation is controlled by the memory effect of STP, and it is mediated primarily by the facilitation time constant. Furthermore, we demonstrated that synaptic facilitation dramatically enhances synchrony propagation in feedforward neural networks and that response timing mediated by synaptic facilitation offers a scheme for information routing. In addition, we verified that synaptic strengthening of intralayer or interlayer coupling enhances synchrony propagation, and we verified that other factors such as the delay of synaptic transmission and the mode of synaptic connectivity are also involved in regulating synchronous activity propagation. Overall, our results highlight the functional role of STP in regulating the inducing and propagation of transient synchronous activity, and they may inspire testable hypotheses for future experimental studies.

Dynamic Configuration of Coactive Micropatterns in the Default Mode Network During Wakefulness and Sleep.

Background: The default mode network (DMN) is a prominent intrinsic network that is observable in many mammalian brains. However, a few studies have investigated the temporal dynamics of this network based on direct physiological recordings. Methods: Herein, we addressed this issue by characterizing the dynamics of local field potentials from the rat DMN during wakefulness and sleep with an exploratory analysis. We constructed a novel coactive micropattern (CAMP) algorithm to evaluate the configurations of rat DMN dynamics, and further revealed the relationship between DMN dynamics with different wakefulness and alertness levels. Results: From the gamma activity (40-80 Hz) in the DMN across wakefulness and sleep, three spatially stable CAMPs were detected: a common low-activity level micropattern (cDMN), an anterior high-activity level micropattern (aDMN), and a posterior high-activity level micropattern (pDMN). A dynamic balance across CAMPs emerged during wakefulness and was disrupted in sleep stages. In the slow-wave sleep (SWS) stage, cDMN became the primary activity pattern, whereas aDMN and pDMN were the major activity patterns in the rapid eye movement sleep stage. In addition, further investigation revealed phasic relationships between CAMPs and the up-down states of the slow DMN activity in the SWS stage. Conclusion: Our study revealed that the dynamic configurations of CAMPs were highly associated with different stages of wakefulness, and provided a potential three-state model to describe the DMN dynamics for wakefulness and alertness. Impact statement In the current study, a novel coactive micropattern (CAMP) method was developed to elucidate fast default mode network (DMN) dynamics during wakefulness and sleep. Our findings demonstrated that the dynamic configurations of DMN activity are specific to different wakefulness stages and provided a three-state DMN CAMP model to depict wakefulness levels, thus revealing a potentially new neurophysiological representation of alertness levels. This work could elucidate the DMN dynamics underlying different stages of wakefulness and have important implications for the theoretical understanding of the neural mechanism of wakefulness and alertness.