钙([Ca2])的生物能量系统,肌醇1,4,5-三磷酸(IP3)和一氧化氮(NO)调节神经元的多种机制。任何或所有钙的失调,IP3和一氧化氮动力学可能导致神经毒性和细胞死亡。文献中很少有关于神经元细胞中[Ca2]与IP3和[Ca2]与一氧化氮的两个系统相互作用的研究,这对神经元细胞的调节和失调过程提供了有限的见解。但是,没有关于三个系统[Ca2+]动力学中串扰的研究,神经元中的IP3和NO。因此,[Ca2+]系统动力学中的串扰,已使用数学模型研究了神经元中IP3和NO的调节过程。[Ca2]和IP3之间的双向反馈过程以及[Ca2]和NO之间通过环磷酸鸟苷(cGMP)和质膜[Ca2]-ATPase(PMCA)的双向反馈过程已纳入所提出的模型。这种耦合自动处理神经元细胞中IP3和一氧化氮之间的间接双向反馈过程。通过使用曲柄-尼科尔森方案(CNS)的有限元方法(FEM)获得了数值结果。结合钠钙交换剂(NCX)和电压门控钙通道(VGCC)的本模型提供了对由于缓冲液而引起的各种调节和失调过程的新颖见解。IP3受体,ryanodine受体,通过PMCA通道的cGMP动力学,等。及其对[Ca2+]交互式时空系统动力学的影响,神经元中的IP3和NO。结论是,对于[Ca2]和NO的两个系统的相互作用以及[Ca2]的三个系统的相互作用,不同关键机制的行为是完全不同的。IP3和一氧化氮在神经元细胞中由于相互调节调节。几种神经系统疾病与钙改变的关联,已经在神经元中探索了IP3和NO。
The bioenergetic system of calcium ([Ca2+]), inositol 1, 4, 5-trisphophate (IP3) and nitric oxide (NO) regulate the diverse mechanisms in neurons. The dysregulation in any or all of the calcium, IP3 and nitric oxide dynamics may cause neurotoxicity and cell death. Few studies are noted in the literature on the interactions of two systems like [Ca2+] with IP3 and [Ca2+] with nitric oxide in neuron cells, which gives limited insights into regulatory and dysregulatory processes in neuron cells. But, no study is available on the cross talk in dynamics of three systems [Ca2+], IP3 and NO in neurons. Thus, the cross talk in the system dynamics of [Ca2+], IP3 and NO regulation processes in neurons have been studied using mathematical model. The two-way feedback process between [Ca2+] and IP3 and two-way feedback process between [Ca2+] and NO through cyclic guanosine monophosphate (cGMP) with plasmalemmal [Ca2+]-ATPase (PMCA) have been incorporated in the proposed model. This coupling handles the indirect two-way feedback process between IP3 and nitric oxide in neuronal cells automatically. The numerical outcomes were acquired by employing the finite element method (FEM) with the Crank-Nicholson scheme (CNS). The present model incorporating the sodium-calcium exchanger (NCX) and voltage-gated calcium channel (VGCC) provides novel insights into the various regulatory and dysregulatory processes due to buffer, IP3-receptor, ryanodine receptor, cGMP kinetics through PMCA channel, etc. and their impacts on the interactive spatiotemporal system dynamics of [Ca2+], IP3 and NO in neurons. It is concluded that the behavior of different crucial mechanisms is quite different for interactions of two systems of [Ca2+] and NO and the interactions of three systems of [Ca2+], IP3 and nitric oxide in neuronal cell due to mutual regulatory adjustments. The association of several neurological disorders with the alterations in calcium, IP3 and NO has been explored in neurons.