Enhanced neurovascular dynamic model for exploring vasoconstriction induced by febrile seizures

Neurovascular coupling is a fundamental concept that elucidates how neuronal electrical activity regulates vascular function, ensuring optimal blood flow to active regions of the brain and optimizing neural function. In this article, we have constructed a novel model of the endothelial Kir2.1 channel that senses potassium ions in the perivascular space and integrated it into a neurovascular coupling model. Our computational framework accounts for the dynamics of neurons, astrocytes, endothelial cells, and smooth muscle cells at the cellular level. By incorporating recent experimental findings, we successfully demonstrate that capillary endothelial cells can detect localized fluctuations in extracellular \(\mathrm {K^+}\) ${\mathrm{K}}^{+}$ concentration through the Kir2.1 channel on their membranes. Subsequently, these cells transmit this signal to smooth muscle cells, initiating the release of vasoactive substances and facilitating vascular motion. This sequence of events forms the core of our model. Furthermore, our simulations support the inclusion of a temperature term in our model, allowing us to accurately replicate experimental observations. This accounts for variations in neuronal electrical activity due to increased temperature, leading to vasoconstriction. In conclusion, our dynamic model serves as a valuable tool for investigating the mechanisms underlying neurovascular coupling and the role of capillary \(\mathrm {K^+}\) ${\mathrm{K}}^{+}$ -sensing in regulating vascular activity. It enhances our understanding of brain function and provides insights for developing therapeutic interventions for neurovascular diseases.