MODELING NEUROVASCULAR COUPLING

The brain critically depends on the uninterrupted vascular supply of oxygen and glucose. Cerebral blood flow is locally regulated by neuronal activity, a process referred to as neurovascular coupling (NVC), which optimizes energy delivery to activated brain regions through the coordinated regulation of vasodilation and vasoconstriction. NVC relies on complex interactions between neurons, astrocytes, and blood vessels. Although vasodilation is better understood, the mechanisms of vasoconstriction remain poorly explored.

To address this gap, we developed minimal differential equation models describing changes in arteriole diameter during vasoconstriction induced by different stimuli. These models were fitted to experimental data obtained from mouse brain slices and accurately captured arteriole contraction dynamics across conditions.

We specifically analyzed vasoconstriction induced by exogenous application of two vasoconstrictors, Prostaglandin E2(PGE2) and Neuropeptide Y(NPY). Beyond reproducing experimental responses, the model enables estimation of free parameters, supporting its validity and predictive power.

We further extended this minimal framework to capture the bidirectional interaction between neuronal activity and vasomotion. By coupling a simplified neuronal activity variable to arteriole diameter dynamics, the model establishes a closed feedback loop in which neuronal activity modulates vascular tone, while vascular changes influence neuronal activity through metabolic supply. Despite its simplicity, this model reproduces essential features of neurovascular feedback and provides a tractable framework to investigate the emergence and stability of activity–vasomotion coupling.

Overall, this study provides a quantitative framework to investigate brain vasoconstriction mechanisms and offers new insights into the role of PGE2 and NPY in NVC under physiological and pathological conditions.