https://doi.org/10.1140/epjp/s13360-023-03691-1
Regular Article
Computational model of calcium dynamics-dependent dopamine regulation and dysregulation in a dopaminergic neuron cell
Department of Mathematics, Bioinformatics and Computer Applications, Maulana Azad National Institute of Technology, 462003, Bhopal, Madhya Pradesh, India
Received:
1
December
2022
Accepted:
10
January
2023
Published online:
16
January
2023
Calcium (Ca2+) signaling is essential for regulating dopamine (DA) concentration levels in neurons. The alterations in the different mechanisms of [Ca2+] dynamics can cause the disturbances in the dopamine regulation in neuron cells. But, no attempt is reported on the spatiotemporal dependence of dopamine regulation on the [Ca2+] dynamics in neurons. A mathematical model is framed to explore the effects of alterations in different processes including source influx, ryanodine receptor, buffer process, serca pump, etc. on the spatiotemporal [Ca2+] and dopamine mechanisms in nerve cells. The Numerical findings have been acquired utilizing finite element techniques and the effects of dysregulation in diverse processes on the spatiotemporal [Ca2+] and dopamine mechanisms in dopaminergic neurons are analyzed. The outcomes provide the better understanding of the regulatory and dysregulatory processes, which can cause the alterations in the spatiotemporal [Ca2+] and dopamine dynamics leading to neuronal diseases such as Parkinson’s, attention deficit hyperactive disorder, depression, schizophrenia, etc. Thus, the present model gives novel information about the specific dysregulatory constitutive mechanisms of calcium and dopamine dynamics like source inflow, buffer, ryanodine receptor, and others, which are responsible for the elevated calcium and dopamine levels, consequently the death of dopaminergic neurons.
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© The Author(s), under exclusive licence to Società Italiana di Fisica and Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
