{"title":"Computational model of the spatiotemporal synergetic system dynamics of calcium, IP3 and dopamine in neuron cells","authors":"Anand Pawar, Kamal Raj Pardasani","doi":"10.1007/s11571-024-10117-w","DOIUrl":null,"url":null,"abstract":"<p>The functioning of several cellular processes in neuron cells relies on the interplay between multiple systems, such as calcium ([Ca<sup>2+</sup>]), inositol 1, 4, 5-trisphosphate (IP<sub>3</sub>), and dopamine. But, their individual dynamics provide very little insight into the various regulatory and dysregulatory cellular processes. The interaction of two systems dynamics offers some useful information about cell functioning in neurons. But, no attempt has been noted in the literature about the cooperation of three systems dynamics of [Ca<sup>2+</sup>], IP<sub>3</sub>, and dopamine in neurons. A mathematical model was utilized to examine the dynamic interactions of [Ca<sup>2+</sup>], IP<sub>3</sub>, and dopamine in neurons, considering their spatiotemporal aspects. Numerical findings were obtained using the finite element technique in conjunction with the Crank–Nicholson scheme. The effects of different component events like IP<sub>3</sub>-receptor (IP<sub>3</sub>R), sodium–calcium exchanger (NCX), calbindin-D<sub>28K</sub> buffer, etc. on the synergetic calcium, IP<sub>3</sub>, and dopamine dynamics have been studied in neuronal cells. The present model offers novel insights into the effects of regulation and dysregulation in different mechanisms like IP<sub>3</sub>R, NCX, calbindin-D<sub>28K</sub>, etc. on the synergetic systems of [Ca<sup>2+</sup>], IP<sub>3</sub> and dopamine in neurons and their association with multiple neurological disorders, including Alzheimer's disease and Parkinson's disease.</p>","PeriodicalId":10500,"journal":{"name":"Cognitive Neurodynamics","volume":"4 1","pages":""},"PeriodicalIF":3.1000,"publicationDate":"2024-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cognitive Neurodynamics","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1007/s11571-024-10117-w","RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
The functioning of several cellular processes in neuron cells relies on the interplay between multiple systems, such as calcium ([Ca2+]), inositol 1, 4, 5-trisphosphate (IP3), and dopamine. But, their individual dynamics provide very little insight into the various regulatory and dysregulatory cellular processes. The interaction of two systems dynamics offers some useful information about cell functioning in neurons. But, no attempt has been noted in the literature about the cooperation of three systems dynamics of [Ca2+], IP3, and dopamine in neurons. A mathematical model was utilized to examine the dynamic interactions of [Ca2+], IP3, and dopamine in neurons, considering their spatiotemporal aspects. Numerical findings were obtained using the finite element technique in conjunction with the Crank–Nicholson scheme. The effects of different component events like IP3-receptor (IP3R), sodium–calcium exchanger (NCX), calbindin-D28K buffer, etc. on the synergetic calcium, IP3, and dopamine dynamics have been studied in neuronal cells. The present model offers novel insights into the effects of regulation and dysregulation in different mechanisms like IP3R, NCX, calbindin-D28K, etc. on the synergetic systems of [Ca2+], IP3 and dopamine in neurons and their association with multiple neurological disorders, including Alzheimer's disease and Parkinson's disease.
期刊介绍:
Cognitive Neurodynamics provides a unique forum of communication and cooperation for scientists and engineers working in the field of cognitive neurodynamics, intelligent science and applications, bridging the gap between theory and application, without any preference for pure theoretical, experimental or computational models.
The emphasis is to publish original models of cognitive neurodynamics, novel computational theories and experimental results. In particular, intelligent science inspired by cognitive neuroscience and neurodynamics is also very welcome.
The scope of Cognitive Neurodynamics covers cognitive neuroscience, neural computation based on dynamics, computer science, intelligent science as well as their interdisciplinary applications in the natural and engineering sciences. Papers that are appropriate for non-specialist readers are encouraged.
1. There is no page limit for manuscripts submitted to Cognitive Neurodynamics. Research papers should clearly represent an important advance of especially broad interest to researchers and technologists in neuroscience, biophysics, BCI, neural computer and intelligent robotics.
2. Cognitive Neurodynamics also welcomes brief communications: short papers reporting results that are of genuinely broad interest but that for one reason and another do not make a sufficiently complete story to justify a full article publication. Brief Communications should consist of approximately four manuscript pages.
3. Cognitive Neurodynamics publishes review articles in which a specific field is reviewed through an exhaustive literature survey. There are no restrictions on the number of pages. Review articles are usually invited, but submitted reviews will also be considered.