GUI Based Modeling and Simulation of Maximal Calcium Ion Bifurcation on Neuron Response and its Applications

In spite of sodium, potassium and chloride ions, calcium, magnesium and cobalt ions also plays a vital role for complex signaling in brain. Calcium ions (Ca
²⁺
) regulate neuronal activity in homo- and hetero cellular control brain physiology. Without calcium ion signaling, all transcriptional networks, and ion exchangers in brain may cause sudden stop of all physiological functions. Wrong interactions between Ca
²⁺
and reactive other species signaling coordinate in neurodegenerative disorders, perturbed energy metabolism, and alterations of disease-related synaptic dysfunction. Therefore, in this paper, review of Ca
²⁺
has been modeled with original H-H equations and discusses deregulation of Ca
²⁺
for different neurological related diseases as Alzheimer, Parkinson, coma etc. These channels activate due to depolarization and inactivate very little and slowly during the whole action potential generation phase. Calcium ion bifurcation was first characterized by Fatt and Katz (1953). From researcher’s simulation and formulation it was concluded, there are various subtypes channel in neuronal cells .These sub-channels serve a vital role in cellular signaling in neuron cell. Based on the neural functionality, calcium ion bifurcation is depended on calcium channel types L
ca
, T
ca
and N
ca
type. L
ca
-type currents are the main calcium ion response observed in muscular cells, where they initiate function of the respective cells. T
ca
type calcium ion response is activated by depolarization of ion. N
ca
type calcium ion channel provided only neuronal activity.This paper represents the bifurcation level of calcium ion response on the neuron functionality and an investigation on the properties of Ca
²⁺
ion response has been observed. This paper also explains the extension of original H-H model for neuron at excitable state and is analyzed with GUI panel with proper simulated version.