@article{Pérez Bonilla_Reyes Monreal_Quintero Pérez_Pérez Escalera_Reyes Lazalde_2021, title={Theoretical Study of the Function of the IP3 Receptor / BK Channel Complex in a Single Neuron}, volume={42}, url={https://rmib.com.mx/index.php/rmib/article/view/1125}, DOI={10.17488/RMIB.42.2.2}, abstractNote={<p>Large conductance calcium-activated potassium (BK) channels carry out many functions in the central nervous system. The opening of BK channels requires a rise in the cytosolic calcium ([Ca<sup>2+</sup>]<sub>cyt</sub>) concentration, which can occur in two ways: calcium influx from voltage-gated calcium channels (VGCCs) located on the plasma membrane and calcium efflux through the endoplasmic reticulum (ER) membrane to the cytosol triggered by inositol 1,4,5-trisphosphate (IP<sub>3</sub>) receptors (IP<sub>3</sub>-Rs) and ryanodine receptors (RyRs). The BK channel/IP<sub>3</sub>-R/RyR interaction has been widely reported in smooth muscle but scarce information exist on neurons, where its presence is uncertain. The aim of this study was to develop a computational model of a neuron to replicate the interaction between the release of Ca<sup>2+</sup> from the ER (through IP<sub>3</sub>-Rs and RyRs) and the opening of BK channels on the plasma membrane to regulate the level of [Ca<sup>2+</sup>]<sub>cyt</sub>, based on the Hodgkin-Huxley formalism and the Goldbeter model. The mathematical models were implemented on Visual Basic® and differential equations were solved numerically. Various conditions of BK conductance and the efflux of endoplasmic Ca<sup>2+</sup> were explored. The results show that an abrupt increase in [Ca<sup>2+</sup>]<sub>cyt</sub> (≥ 5 mM) activates the BK channels and either pauses or stops the action potential train.</p>}, number={2}, journal={Revista Mexicana de Ingenieria Biomedica}, author={Pérez Bonilla, María Eugenia and Reyes Monreal, Marleni and Quintero Pérez, Jessica and Pérez Escalera, Miguel and Reyes Lazalde, Arturo}, year={2021}, month={Mar.}, pages={15–31} }