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.

中文翻译：

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来自三个神经元系统前馈抑制网络的神经血管耦合产生的NIRS和BOLD信号的计算分析。

由于大脑功能缺损引起的大脑缺氧状态，会发生几种神经系统疾病，这可以通过星形胶质细胞中生物反应介导的神经刺激驱动的血管活性反应来控制，这种现象称为神经血管耦合。在这种机制的帮助下，大脑可以通过引起血管舒张来适应低氧状况。为了推断由神经元刺激引起的血管舒张的机制，目前的研究阐明了一种数学模型，该模型涉及神经元系统前馈抑制网络模型（FFI）与神经血管耦合的其他两个功能成分，即星形胶质细胞和平滑肌细胞衬里血管。该研究包括神经抑制网络系统，其中谷氨酸能锥体神经元和GABA能中间神经元相互拮抗。所提出的模型成功地包含了抑制系统的含义，以设计用于神经血管耦合的数学模型。该模型的结果表明，神经元刺激从20 µA / cm2增加到60 µA / cm2，具有增加血液组织脉管血管舒张活性的能力。通过局部脑氧合水平（rSO2）和依赖于血氧水平（BOLD）的成像信号，计算了由于输入突触刺激而引起的氧合水平和血液动力学响应，该信号支持随着突触输入刺激的增加而使血管舒张。所提出的模型成功地包含了抑制系统的含义，以设计用于神经血管耦合的数学模型。该模型的结果表明，神经刺激从20 µA / cm2增加到60 µA / cm2，具有增加血液组织脉管血管舒张活性的能力。通过局部脑氧合水平（rSO2）和依赖于血氧水平（BOLD）的成像信号，计算了由于输入突触刺激而引起的氧合水平和血液动力学响应，该信号支持随着突触输入刺激的增加而使血管舒张。所提出的模型成功地包含了抑制系统的含义，以设计用于神经血管耦合的数学模型。该模型的结果表明，神经刺激从20 µA / cm2增加到60 µA / cm2，具有增加血液组织脉管血管舒张活性的能力。通过局部脑氧合水平（rSO2）和依赖于血氧水平（BOLD）的成像信号，计算了由于输入突触刺激而引起的氧合水平和血液动力学响应，该信号支持随着突触输入刺激的增加而使血管舒张。