Speaker
Description
The brain critically depends on a continuous vascular supply of oxygen and glucose. Cerebral blood flow is locally regulated by neuronal activity through neurovascular coupling (NVC), a mechanism that optimizes energy delivery to active brain regions via coordinated vasodilation and vasoconstriction. NVC arises from interactions between neurons, astrocytes, and blood vessels. While vasodilation has been extensively studied, the mechanisms underlying vasoconstriction remain less understood.
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 from mouse brain slices and accurately reproduced arteriole contraction dynamics across conditions.
We specifically analyzed vasoconstriction induced by Prostaglandin E2 (PGE2) and Neuropeptide Y (NPY). Beyond reproducing experimental responses, the model enables estimation of free parameters, supporting its predictive capacity. We further extended this framework to capture the bidirectional interaction between neuronal activity and vasomotion, coupling a neuronal activity variable to arteriole diameter dynamics and forming a closed feedback loop between neuronal demand and vascular tone.
