Computational analysis of NIRS and BOLD signal from neurovascular coupling with three neuron-system feedforward inhibition network

Abstract

Several neurological disorders occur due to hypoxic condition in brain arising from impairment of cerebral functionality, which can be controlled by neural stimulation driven vasoactive response mediated through biological response in astrocyte, a phenomenon known as neurovascular coupling. Brain can adjust with the problem of hypoxic condition by causing vasodilation with the help of this mechanism. To deduce the mechanism behind vasodilation of blood vessel caused by neuronal stimulus, current study articulates a mathematical model involving neuronal system feedforward inhibition network model (FFI) with two other functional components of neurovascular coupling, i.e. astrocyte and smooth muscle cell lining blood vessel. This study includes the neural inhibition network system where glutamatergic pyramidal neuron and GABAergic interneuron act antagonistically with each other. The proposed model successfully includes the implication of the inhibition system to design mathematical model for neurovascular coupling. Result of the proposed model shows that the increase in neuronal stimulus from 20 to 60 µA/cm² has the ability to increase the vasodilatory activity of blood tissue vasculature. Oxygenation level and hemodynamic response due to input synaptic stimulation has been calculated by regional cerebral oxygenation level (rS0₂) and blood oxygen level dependent (BOLD) imaging signal which supports vasodilation of blood vessel with increase in synaptic input stimulus.

Keywords: Feedforward-inhibition network; Hodgkin-Huxley model; Neurotransmitter; Neurovascular coupling unit; Regional cerebral oxygen saturation.