Soft neural electrode arrays that are mechanically matched between neural tissues and electrodes offer valuable opportunities for the development of disease diagnose and brain computer interface systems. Here, a thermal release transfer printing method for fabrication of stretchable bioelectronics, such as soft neural electrode arrays, is presented. Due to the large, switchable and irreversible change in adhesion strength of thermal release tape, a low‐cost, easy‐to‐operate, and temperature‐controlled transfer printing process can be achieved. The mechanism of this method is analyzed by experiments and fracture‐mechanics models. Using the thermal release transfer printing method, a stretchable neural electrode array is fabricated by a sacrificial‐layer‐free process. The ability of the as‐fabricated electrode array to conform different curvilinear surfaces is confirmed by experimental and theoretical studies. High‐quality electrocorticography signals of anesthetized rat are collected with the as‐fabricated electrode array, which proves good conformal interface between the electrodes and dura mater. The application of the as‐fabricated electrode array on detecting the steady‐state visual evoked potentials research is also demonstrated by in vivo experiments and the results are compared with those detected by stainless‐steel screw electrodes.
The importance of self-feedback autaptic transmission in modulating spike-time irregularity is still poorly understood. By using a biophysical model that incorporates autaptic coupling, we here show that self-innervation of neurons participates in the modulation of irregular neuronal firing, primarily by regulating the occurrence frequency of burst firing. In particular, we find that both excitatory and electrical autapses increase the occurrence of burst firing, thus reducing neuronal firing regularity. In contrast, inhibitory autapses suppress burst firing and therefore tend to improve the regularity of neuronal firing. Importantly, we show that these findings are independent of the firing properties of individual neurons and as such can be observed for neurons operating in different modes. Our results provide an insightful mechanistic understanding of how different types of autapses shape irregular firing at the single-neuron level and they highlight the functional importance of autaptic self-innervation in taming and modulating neurodynamics.
18 June 2018 in IEEE Transactions on Neural Systems and Rehabilitation Engineering
A canonical correlation analysis (CCA) is a state-of-the-art method for frequency recognition in steady-state visual evoked potential (SSVEP)-based brain-computer interface (BCI) systems. Various extended methods have been developed, and among such methods, a combination method of CCA and individual-template-based CCA has achieved the best performance. However, the CCA requires the canonical vectors to be orthogonal, which may not be a reasonable assumption for the EEG analysis. In this paper, we propose using the correlated component analysis (CORRCA) rather than CCA to implement frequency recognition. CORRCA can relax the constraint of canonical vectors in CCA and generate the same projection vector for two multichannel EEG signals. Furthermore, we propose a two-stage method based on the basic CORRCA method (termed TSCORRCA). Evaluated on a benchmark data set of 35 subjects, the experimental results demonstrate that CORRCA significantly outperformed CCA, and TSCORRCA obtained the best performance among the compared methods. This paper demonstrates that CORRCA-based methods have a great potential for implementing high-performance SSVEP-based BCI systems.
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. One prevailing viewpoint on the genesis of absence seizures is suggested to involve the pathological interactions within the corticothalamic system. As intriguing deep nuclei of brain, the basal ganglia are reported to play crucial roles in controlling absence seizures through multiple nigro-thalamic pathways. Beside these nigro-thalamic pathways, recent experiments have identified a new direct GABAergic pallido-cortical pathway projecting from the globus pallidus externa (GPe) to the cerebral cortex. Does this novel identified inhibitory pallido-cortical pathway also participate in regulating absence seizures? By computational modelling, we demonstrated that this inhibitory pallido-cortical pathway indeed participates in the control of absence seizures. Specifically, both activating the GPe neurons and enhancing the strength of this pathway significantly inhibit the typical 2–4 Hz spike and wave discharges (SWDs) during absence seizures. Further investigation showed that appropriate tuning of several GPe-related pathways may trigger the SWD suppression by activating GPe neurons, and also the strength of this inhibitory pallido-cortical pathway may regulate the so-called bidirectional control of absence seizures caused by direct nigro-thalamic pathways. These results highlight the functional roles of the GABAergic pallido-cortical pathway in controlling absence seizures and have important physiological implications in the treatment of absence epilepsy.
26 May 2023 in IEEE Transactions on Cognitive and Developmental Systems
Spiking neural networks (SNNs) have demonstrated excellent capabilities in various intelligent scenarios. Most existing methods for training SNNs are based on the concept of synaptic plasticity; however, learning in the realistic brain also utilizes intrinsic non-synaptic mechanisms of neurons. The spike threshold of biological neurons is a critical intrinsic neuronal feature that exhibits rich dynamics on a millisecond timescale and has been proposed as an underlying mechanism that facilitates neural information processing. In this study, we develop a novel synergistic learning approach that involves simultaneously training synaptic weights and spike thresholds in SNNs. SNNs trained with synapse-threshold synergistic learning (STL-SNNs) achieve significantly superior performance on various static and neuromorphic datasets than SNNs trained with two degenerated single-learning models. During training, the synergistic learning approach optimizes neural thresholds, providing the network with stable signal transmission via appropriate firing rates. Further analysis indicates that STL-SNNs are robust to noisy data and exhibit low energy consumption for deep network structures. Additionally, the performance of STL-SNN can be further improved by introducing a generalized joint decision framework. Overall, our findings indicate that biologically plausible synergies between synaptic and intrinsic non-synaptic mechanisms may provide a promising approach for developing highly efficient SNN learning methods.