A bidirectional model for communication in the neurovascular unit.

The neurovascular unit is a coordinated and interactional system of neurons, astrocytes, and microvessels in the brain. A central autoregulation mechanism observed in this unit is functional hyperemia, in which the microvasculature dilates in response to local neural activity in order to meet the increased demand for blood flow and oxygen. We have developed the first interactional model of bidirectional signaling in the neurovascular unit. The vascular model includes a description of vasomotion, the vascular oscillatory response to transmural pressure, observed in vivo. The communication mechanisms in the model include neural synaptic glutamate and potassium signaling to the astrocytes, potassium signaling from the astrocyte to the microvasculature, and astrocytic mechanosensation of vascular changes. The model response of the astrocyte to arteriolar dilation is validated with recent in vivo and in vitro experimental results. The model reproduces for the first time the in vitro observed phenomenon in which arteriole radius and Ca(2+) oscillations, "vasomotion," are damped due to neural induced astrocytic signaling.