| | Models | Description |
| 1. |
A model for pituitary GH(3) lactotroph (Wu and Chang 2005)
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The ATP-sensitive K(+) (K(ATP)) channels are composed of sulfonylurea receptor and inwardly rectifying K(+) channel (Kir6.2) subunit. These channels are regulated by intracellular ADP/ATP ratio and play a role in cellular metabolism. ... The objective of this study was to determine whether Diethyl pyrocarbonate (DEPC) modifies K(ATP)-channel activity in pituitary GH(3) cells. ... Simulation studies also demonstrated that the increased conductance of K(ATP)-channels used to mimic DEPC actions reduced the frequency of spontaneous action potentials and fluctuation of intracellular Ca(2+). The results indicate that chemical modification with DEPC enhances K(ATP)-channel activity and influences functional activities of pituitary GH(3) cells. See paper for more and details. |
| 2. |
Action potential of mouse urinary bladder smooth muscle (Mahapatra et al 2018)
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Urinary incontinence is associated with enhanced spontaneous phasic contractions of the detrusor smooth muscle (DSM). Although a complete understanding of the etiology of these spontaneous contractions is not yet established, it is suggested that the spontaneously evoked action potentials (sAPs) in DSM cells initiate and modulate the contractions. In order to further our understanding of the ionic mechanisms underlying sAP generation, we present here a biophysically detailed computational model of a single DSM cell. First, we constructed mathematical models for nine ion channels found in DSM cells based on published experimental data: two voltage-gated Ca2+ ion channels, an hyperpolarization-activated ion channel, two voltage-gated K+ ion channels, three Ca2+-activated K+ ion channels and a non-specific background leak ion channel. Incorporating these channels, our DSM model is capable of reproducing experimentally recorded spike-type sAPs of varying configurations, ranging from sAPs displaying after-hyperpolarizations to sAPs displaying after-depolarizations. Our model, constrained heavily by physiological data, provides a powerful tool to investigate the ionic mechanisms underlying the genesis of DSM electrical activity, which can further shed light on certain aspects of urinary bladder function and dysfunction. |
| 3. |
CA1 pyramidal neuron to study INaP properties and repetitive firing (Uebachs et al. 2010)
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A model of a CA1 pyramidal neuron containing a biophysically realistic morphology and 15 distributed voltage and Ca2+-dependent conductances. Repetitive firing is modulated by maximal conductance and the
voltage dependence of the persistent Na+ current (INaP). |
| 4. |
Contribution of ATP-sensitive potassium channels in the neuronal network (Huang et al. 2009)
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Epileptic seizures in diabetic hyperglycemia (DH) are not uncommon.
This study aimed to determine the acute behavioral, pathological, and electrophysiological effects of status epilepticus (SE) on diabetic animals.
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We also used a simulation model to evaluate intracellular adenosine triphosphate (ATP) and neuroexcitability.
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In the simulation, increased intracellular ATP concentration promoted action potential firing.
This finding that rats with DH had more brain damage after SE than rats without diabetes suggests the importance of intensively treating hyperglycemia and seizures in diabetic patients with epilepsy. |
| 5. |
Effects of eugenol on the firing of action potentials in NG108-15 neurons (Huang et al. 2011)
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"Rationale: Eugenol (EUG, 4-allyl-2-methoxyphenol), the main component of essential oil extracted from cloves, has various uses in medicine because of its potential to modulate neuronal excitability.
However, its effects on the ionic mechanisms remains incompletely understood.
Objectives: We aimed to investigate EUG`s effects on neuronal ionic currents and excitability, especially on voltage-gated ion currents, and to verify the effects on a hyperexcitability-temporal lobe seizure model.
Methods: With the aid of patch-clamp technology, we first investigated the effects of EUG on ionic currents in NG108-15 neuronal cells differentiated with cyclic AMP. We then used modified Pinsky-Rinzel simulation modeling to evaluate its effects on spontaneous action potentials (APs).
Finally, we investigated its effects on pilocarpine-induced seizures in rats.
Results: EUG depressed the transient and late components of INa in the neurons.
It not only increased the degree of INa inactivation, but specifically suppressed the non-inactivating INa (INa(NI)).
... In addition, EUG diminished L-type Ca2+ current and delayed rectifier K+ current only at higher concentrations. EUG`s effects on APs frequency reduction was verified by the simulation modeling.
In pilocarpine-induced seizures, the EUG-treated rats showed no shorter seizure latency but a lower seizure severity and mortality than the control rats.
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Conclusion: The synergistic blocking effects of INa and INa(NI) contributes to the main mechanism through which EUG affects the firing of neuronal APs and modulate neuronal hyperexcitability such as pilocarpine-induced temporal lobe seizures." |
| 6. |
Integrated Oscillator Model for pancreatic islet beta-cells (Marinelli et al., 2022)
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This version of the Integrated Oscillator Model for pancreatic beta-cells includes variables for oxidative phosphorylation, as well as glycolysis, electrical activity, and calcium dynamics. |
| 7. |
Model for K-ATP mediated bursting in mSNc DA neurons (Knowlton et al 2018)
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"Burst firing in medial substantia nigra dopamine (mSN DA) neurons has been selectively linked to novelty-induced exploration behavior in mice. Burst firing in mSN DA neurons, in contrast to lateral SN DA neurons, requires functional ATP-sensitive potassium channels (K-ATP) both in vitro and in vivo. However, the precise role of K-ATP channels in promoting burst firing is un-known. We show experimentally that L-type calcium channel activity in mSN DA neurons en-hances open probability of K-ATP channels. We then generated a mathematical model to study the role of Ca2+ dynamics driving K-ATP channel function in mSN DA neurons during bursting. ..." |
| 8. |
Model for pancreatic beta-cells with two isoforms of PFK (Marinelli et al., 2022)
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This version of the Integrated Oscillator Model has two PFK isoforms, as well as modules for oxidative phosphorylation, electrical activity, and intracellular calcium. |
| 9. |
Model for pusatile insulin secretion at basal levels of glucose (Fletcher et al, 2022)
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This model describes the basis of pulsatile insulin secretion from islet beta-cells at basal levels of glucose, where the cells are not electrically active. |
| 10. |
Pancreatic Beta Cell signalling pathways (Fridlyand & Philipson 2016) (MATLAB)
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This is a 3rd party implementation of Fridlyand & Philipson 2016 who's abstract begins "Insulin secretory in pancreatic beta-cells responses to nutrient
stimuli and hormonal modulators include multiple messengers and
signaling pathways with complex interdependencies. Here we present a
computational model that incorporates recent data on glucose
metabolism, plasma membrane potential, G-protein-coupled-receptors
(GPCR), cytoplasmic and endoplasmic reticulum calcium dynamics, cAMP
and phospholipase C pathways that regulate interactions between second
messengers in pancreatic beta-cells. The values of key model
parameters were inferred from published experimental data. The model
gives a reasonable fit to important aspects of experimentally measured
metabolic and second messenger concentrations and provides a framework
for analyzing the role of metabolic, hormones and neurotransmitters
changes on insulin secretion. Our analysis of the dynamic data
provides support for the hypothesis that activation of Ca2+-dependent
adenylyl cyclases play a critical role in modulating the effects of
glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic
polypeptide (GIP) and catecholamines. ..." |
| 11. |
The role of ATP-sensitive potassium channels in a hippocampal neuron (Huang et al. 2007)
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"Hyperglycemia-related neuronal excitability and epileptic seizures
are not uncommon in clinical practice. However, their underlying
mechanism remains elusive. ATP-sensitive K(+) (K(ATP)) channels are
found in many excitable cells, including cardiac myocytes,
pancreatic beta cells, and neurons. These channels provide a link
between the electrical activity of cell membranes and cellular
metabolism. We investigated the effects of higher extracellular
glucose on hippocampal K(ATP) channel activities and neuronal
excitability. The cell-attached patch-clamp configuration on
cultured hippocampal cells and a novel multielectrode recording
system on hippocampal slices were employed. In addition, a
simulation modeling hippocampal CA3 pyramidal neurons (Pinsky-Rinzel
model) was analyzed to investigate the role of K(ATP) channels in
the firing of simulated action potentials. ..." |
| 12. |
Ventricular cell model (Luo Rudy dynamic model) (Luo Rudy 1994) used in (Wang et al 2006) (XPP)
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A mathematical model of the membrane action potential of the mammalian ventricular cell introduced in Luo, Rudy 1991 and used in Wang et al 2006 is made available here in XPP. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. ... The results are consistent with recent experimental observations, and the model simulations relate these phenomena to the underlying ionic channel kinetics. See papers for more and details. |
