Frontiers in Computational Neuroscience最新文献

Introduction: Understanding the cognitive process of thinking as a neural phenomenon remains a central challenge in neuroscience and computational modeling. This study addresses this challenge by presenting a biologically grounded framework that simulates adaptive decision making across cognitive states.

Methods: The model integrates neuronal synchronization, metabolic energy consumption, and reinforcement learning. Neural synchronization is simulated using Kuramoto oscillators, while energy dynamics are constrained by multimodal activity profiles. Reinforcement learning agents-Q-learning and Deep Q-Network (DQN)-modulate external inputs to maintain optimal synchrony with minimal energy cost. The model is validated using real EEG and fMRI data, comparing simulated and empirical outputs across spectral power, phase synchrony, and BOLD activity.

Results: The DQN agent achieved rapid convergence, stabilizing cumulative rewards within 200 episodes and reducing mean synchronization error by over 40%, outperforming Q-learning in speed and generalization. The model successfully reproduced canonical brain states-focused attention, multitasking, and rest. Simulated EEG showed dominant alpha-band power (3.2 × 10^-4 a.u.), while real EEG exhibited beta-dominance (3.2 × 10^-4 a.u.), indicating accurate modeling of resting states and tunability for active tasks. Phase Locking Value (PLV) ranged from 0.9806 to 0.9926, with the focused condition yielding the lowest circular variance (0.0456) and a near significant phase shift compared to rest (t = -2.15, p = 0.075). Cross-modal validation revealed moderate correlation between simulated and real BOLD signals (r = 0.30, resting condition), with delayed inputs improving temporal alignment. General Linear Model (GLM) analysis of simulated BOLD data showed high region-specific prediction accuracy (R ² = 0.973-0.993, p < 0.001), particularly in prefrontal, parietal, and anterior cingulate cortices. Voxel-wise correlation and ICA decomposition confirmed structured network dynamics.

Discussion: These findings demonstrate that the framework captures both electrophysiological and spatial aspects of brain activity, respects neuroenergetic constraints, and adaptively regulates brain-like states through reinforcement learning. The model offers a scalable platform for simulating cognition and developing biologically inspired neuroadaptive systems.

Conclusion: This work provides a novel and testable approach to modeling thinking as a biologically constrained control problem and lays the groundwork for future applications in cognitive modeling and brain-computer interfaces.

Introduction: Parkinson's disease (PD) is the fastest-growing neurodegenerative disorder, with subtle gait changes such as reduced vertical ground-reaction forces (VGRF) often preceding motor symptoms. These gait abnormalities, measurable via wearable VGRF sensors, offer a non-invasive means for early PD detection. However, current computational approaches often suffer from redundant features and class imbalance, limiting both accuracy and generalizability.

Methods: We propose CRISP (Correlation-filtered Recursive Feature Elimination and Integration of SMOTE Pipeline for Gait-Based Parkinson's Disease Screening), a lightweight multistage framework that sequentially applies correlation-based feature pruning, recursive feature elimination (RFE), and Synthetic Minority Oversampling Technique (SMOTE) based class balancing. To ensure clinically meaningful evaluation, a novel subject-wise protocol was also introduced that assigns one prediction per individual enhancing patient-level variability capture and better aligning with diagnostic workflows. Using 306 VGRF recordings (93 PD, 76 controls), five classifiers, i.e., k-Nearest Neighbours (KNN), Decision Tree (DT), Random Forest (RF), Gradient boosting (GB), and Extreme Gradient Boosting (XGBoost) were evaluated for both binary PD detection and multiclass severity grading.

Results: CRISP consistently improved performance across all models under 5-fold cross-validation. XGBoost achieved the highest performance, increasing subject-wise PD detection accuracy from 96.1 ± 0.8% to 98.3 ± 0.8%, and severity grading accuracy from 96.2 ± 0.7% to 99.3 ± 0.5%.

Conclusion: CRISP is the first VGRF-based pipeline to combine correlation-filtered feature pruning, recursive feature elimination, and SMOTE to enhance PD detection performance, while also introducing a subject-wise evaluation protocol that captures patient-level variability for truly personalized diagnostics. These twin novelties deliver clinically significant gains and lay the foundation for real-time, on-device PD detection and severity monitoring.

Introduction: Predictive processing posits that the brain minimizes discrepancies between internal predictions and sensory inputs, offering a unifying account of perception, cognition, and action. In voluntary actions, it is thought to suppress self-generated sensory outcomes. Although sensory mismatch signals have been extensively investigated and modeled, mechanistic insights into the neural computation of predictive processing in voluntary actions remain limited.

Methods: We developed a computational model comprising two-compartment excitatory pyramidal cells (PCs) and three major types of inhibitory interneurons with biologically realistic connectivity. The model incorporates experience-dependent inhibitory plasticity and feature selectivity to shape excitation-inhibition (E/I) balance. We then extended it to a two-dimensional prediction-error (PE) circuit in which each PC has two segregated, top-down modulated dendrites-each bell-tuned to a distinct feature-enabling combination selectivity.

Results: The model reveals that top-down predictions can selectively suppress PCs with matching feature selectivity via experience-dependent inhibitory plasticity. This suppression depends on the response selectivity of inhibitory interneurons and on balanced excitation and inhibition across multiple pathways. The framework also accommodates predictions involving two independent features.

Discussion: By combining biological connectivity data with computational modeling, this study provides insights into the neural circuits and computations underlying the active suppression of sensory responses in voluntary actions. These findings contribute to understanding how the brain generates and processes predictions to guide behavior.

Introduction: Understanding how neurons respond to time-varying electric fields is essential for both basic neuroscience and the development of neuromodulation strategies. However, the mechanisms by which alternating-current induced electric fields (AC-IEF) influence neuronal sensitivity and firing remain unclear.

Methods: We developed a modified two-compartment Pinsky-Rinzel (PR) neuron model incorporating AC-IEF stimulation. Using systematic simulations, we examined firing responses across a wide range of field frequencies, amplitudes, and intrinsic membrane parameters, including inter-compartmental conductance and potassium reversal potential.

Results: Neurons exhibited no firing or sensitivity when the field amplitude was less than twice the baseline membrane potential, regardless of conductance or reversal potential. Sensitivity increased markedly with amplitude: for example, when the amplitude exceeded 0.5 mV/cm, maximum firing rates rose by up to 45% and the sensitivity frequency range extended to 10-50 Hz. Phase-locking phenomena (1:1 and 2:1) were observed, with bandwidths widening as amplitude increased. For amplitudes below 30 mV, firing pattern transitions depended strongly on inter-compartmental conductance, whereas amplitudes ≥30 mV produced a consistent progression ending in subthreshold oscillations. Similar parameter-dependent transitions occurred for different potassium reversal potentials, converging at high amplitudes.

Discussion: These results reveal a parameter-dependent mechanism by which AC-IEF modulate neuronal excitability. The findings provide qualitative rather than strictly quantitative insights into how external electromagnetic environments can shape neural activity, offering new directions for targeted neuromodulation in both health and disease.

Hippocampal neurons generate membrane potential resonance due to specific voltage-gated ion channels, known as resonating conductances, which play crucial physiological roles. However, it is not known whether this phenomenon of resonance is limited to membrane voltage or whether it propagates through molecular signaling components such as calcium dynamics. To test this, we first utilized a single-compartment model neuron to study the oscillatory intrinsic calcium response dynamics of hippocampal model neurons, and the effects of T-type calcium channel kinetics on the voltage and calcium resonance. We found that in the presence of T-type calcium channels, our model neuron sustained a strong calcium resonance compared to voltage resonance. Unlike voltage resonance, calcium resonance frequency was largely independent of conductance magnitude, and the two types of resonance were dissociated, meaning independent of each other. In addition, we studied the effects of A-type K⁺-channels and h-channels in conjunction with T-type calcium channels on calcium resonance, and showed that these two types of channels differentially affect calcium resonance. Finally, using a multi-compartmental morphologically realistic neuron model, we studied calcium resonance along the somato-apical dendritic axis. Using this model, we found that calcium resonance frequency remains almost constant along the somato-apical trunk for the most part, and only toward its terminal end, the calcium resonance frequency was increased. Nonetheless, this increase was lesser compared to the increase in voltage resonance frequency. Our study opens new horizons in the field of molecular resonance, and deepen our understanding concerning the effects of frequency-based neurostimulation therapies, such as transcranial alternating current stimulation (tACS).

Introduction: People with post-stroke aphasia (PSA) exhibit significant interindividual variability attributed to distinctive network disruption patterns across individuals. This complexity limits the effectiveness of conventional one-size-fits-all brain stimulation approaches, but to date no individualized tACS targeting on functional network was studied in PSA. This two-phase study aimed to investigate the immediate network-modulation and language-facilitation effects of dual-site in-phase tACS utilizing a novel individualized targeting method based on individual's EEG dysfunctome.

Methods: In the first phase, network-based linear regression was used to identify aphasia-severity-predictive dysfunctome from the speech-production EEG data of 15 Cantonese-speaking people with aphasia (PWA). Individualized stimulation targets were determined using two targeting principles. Restoration-based targeting aims to restore a target edge which is centralized within the target dysfunctome but weakly-connected in the individual, whereas enhancement-based targeting selects a strongly-connected target edge. The second phase involved a single-session double-blinded sham-controlled trial with the same group to evaluate the immediate effects of dual-site 7-Hz 1-mA tACS under four conditions: Restoration In-phase (RI), Enhancement In-phase (EI), Enhancement Anti-phase (EA), and Sham (SH).

Results: In the first phase, we explored a range of frequency bands and EEG tasks and identified a left frontal-temporal theta network under divergent naming task that significantly predicted aphasia severity. The single-session clinical trial in the second phase demonstrated that RI condition produced increases in the target node strength, global network properties, and divergent naming performance, which were absent in sham and the other two real stimulation conditions.

Discussion: This was the first-of-its-kind dysfunctome-based data-driven individualized tACS demonstrated immediate neuromodulatory effects in PSA. The findings suggest that EEG dysfunctome can help pinpointing effective individualized targets for tACS to promote clinically-beneficial functional reorganization. Despite limited generalizability due to the small sample, this methodology holds significant potential for application in longer-term treatment and other network-based disorders.

Fitting models to experimental intracellular data is challenging. While detailed conductance-based models are difficult to train, phenomenological statistical models often fail to capture the rich intrinsic dynamics of circuits such as central pattern generators (CPGs). A recent trend has been to employ tools from deep learning to obtain data-driven models that can quantitatively learn intracellular dynamics from experimental data. This paper addresses the general questions of modeling, training, and interpreting a large class of such models in the context of estimating the dynamics of a neural circuit. In particular, we use recently introduced Recurrent Mechanistic Models to predict the dynamics of a Half-Center Oscillator (HCO), a type of CPG. We construct the HCO by interconnecting two neurons in the Stomatogastric Ganglion using the dynamic clamp experimental protocol. This allows us to gather ground truth synaptic currents, which the model is able to predict-even though these currents are not used during training. We empirically assess the speed and performance of the training methods of teacher forcing, multiple shooting, and generalized teacher forcing, which we present in a unified fashion tailored to data-driven models with explicit membrane voltage variables. From a theoretical perspective, we show that a key contraction condition in data-driven dynamics guarantees the applicability of these training methods. We also show that this condition enables the derivation of data-driven frequency-dependent conductances, making it possible to infer the excitability profile of a real neuronal circuit using a trained model.