Open AccessTheoretical Study of the Function of the IP3 Receptor / BK Channel Complex in a Single Neuron
Author(s) -
M. E. Pérez-Bonilla,
M. Reyes-Monreal,
Jessica Quintero-Pérez,
Miguel Pérez-Escalera,
A. Reyes-Lazalde
Publication year - 2021
Language(s) - English
Resource type - Dissertations/theses
DOI - 10.17488/rmib.42.2.2
Subject(s) - bk channel , ryanodine receptor , endoplasmic reticulum , biophysics , cytosol , chemistry , inositol , calcium , calcium signaling , inositol trisphosphate receptor , receptor , microbiology and biotechnology , neuroscience , potassium channel , biology , biochemistry , organic chemistry , enzyme
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 ([Ca2+]cyt) 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 (IP3) receptors (IP3-Rs) and ryanodine receptors (RyRs). The BK channel/IP3-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 Ca2+ from the ER (through IP3-Rs and RyRs) and the opening of BK channels on the plasma membrane to regulate the level of [Ca2+]cyt, 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 Ca2+ were explored. The results show that an abrupt increase in [Ca2+]cyt (≥ 5 mM) activates the BK channels and either pauses or stops the action potential train.