Inhibition of spike-wave discharges (SWD) was thought to be associated with remission of seizure symptoms in absence epilepsy. In the previous studies, pulse stimulation was applied directly to the brain as an effective means to inhibit SWD. However, this method not only failed to provide a real-time tracking control of the disease, but also caused incalculable damage to the patient's brain tissue. To fill the gap, this work studied the mitigation and elimination effects of SWD by applying single-pulse coordinated resetting stimulation (SCRS) to three different neurons, firstly. Secondly, based on the 2I:2O cortical-thalamic model (2I:2O SCT model), four kinds of m:n on-off SCRS with the same period were compared, and the control efficiency and impulse energy consumption were combined to investigate these different stimulations. Finally, we further optimized the regulation strategies, including the weighted structure of stimulation and closed-loop control. Simulation results show that the weighted stimulation and closed-loop control strategy proposed here further improve control performance by reducing energy consumption, which may be more reliable in applications. Moreover, this study provides a new method for optimizing SCRS by the weighted processing and closed-loop control of electrical pulses to alleviate the absence epileptic state.

The role of excitatory interneurons (EINs) in the cortical has received increasing attention in the discussion of absence seizures. Numerous physiological experiments have confirmed the correlation between EIN and absence seizures. However, the dynamic mechanisms underlying this relationship are not well understood, and there are some challenges in selecting appropriate stimulation strategies for pyramidal clusters. In this study, we incorporated EIN into the previous Taylor model and developed an improved thalamocortical coupled model consisting of ten neuronal populations. Initially, we investigated the excitatory induction effect of EIN to pyramidal clusters and the external input of EIN. Then, four different targeted treatment approaches (deep brain stimulation (DBS), current balanced biphasic pulse (CBBP), 1:0 coordinated resetting stimulation (1:0 CRS), and 3:2 CRS) were applied to the pyramidal clusters. Moreover, we established two quantitative indices to evaluate the stimulation effects. The results showed that modifying the external input of EIN and the coupling strength projected onto the pyramidal clusters can effectively transition the system from an absence seizure state to other normal states. Additionally, inputs from the left compartment were found to reduce the generation of abnormal discharge regions in the right compartment. Furthermore, considering the treatment effects and current consumption, the 3:2 CRS stimulation strategy appeared to be the most suitable treatment approach for the pyramidal clusters. This work introduces a novel coupled model containing EIN, which contributes new theoretical foundations and insights for the future treatment of absence seizures.

Patients with congenital analgesia who lack the ability to sense temperature generally face low survival rates, highlighting a critical need to understand the underlying mechanisms of heat sensation. While previous research has focused on modeling neural responses to stimuli, the specific mechanisms by which heat-sensitive neurons respond to external temperature changes remain unclear. This gap in knowledge is particularly relevant, as identifying how these neurons react to diverse stimuli can provide insight into sensory deficits linked to congenital analgesia. In this study, we developed a model of heat-sensitive neurons based on the FitzHugh-Nagumo (FHN) neural circuit to investigate neuronal response patterns to external heat stimuli. Two distinct stimulus patterns, each combined with Gaussian white noise, were applied to the model to induce varied firing modes. By calculating the Hamilton energy for each firing mode, we quantified the impact of each external stimulus on neuronal activity. A correlation function was further defined to explore how different stimuli influence the selection of firing modes. Simulation results demonstrate that heat-sensitive neurons show a preferential response to stimuli that induce spike discharge over stimuli that induce r-clonic patterns, as seen in changes to the periodic attractor contours. When exposed to Chua's circuit stimulus, chaotic emission patterns reveal significant shifts in attractor contour, indicating a strong response to spike, r-clonic, and periodic stimuli. These findings suggest that external stimuli capable of inducing spike-and-wave or r-clonic patterns are sensitively detected by thermosensitive neurons, leading to heightened Hamilton energy release and increased regularity in neural activity. This study enhances our understanding of thermosensitive neuronal dynamics under complex stimuli, shedding light on potential response mechanisms relevant to sensory dysfunction in congenital analgesia and advancing the broader field of neural response modeling.