000145140 001__ 145140
000145140 005__ 20241220120715.0
000145140 0247_ $$2doi$$a10.1113/JP285950
000145140 0248_ $$2sideral$$a140004
000145140 037__ $$aART-2024-140004
000145140 041__ $$aeng
000145140 100__ $$aBartolucci, Chiara
000145140 245__ $$aComputational modelling of mouse atrio ventricular node action potential and automaticity
000145140 260__ $$c2024
000145140 5060_ $$aAccess copy available to the general public$$fUnrestricted
000145140 5203_ $$aThe atrioventricular node (AVN) is a crucial component of the cardiac conduction system. Despite its pivotal role in regulating the transmission of electrical signals between atria and ventricles, a comprehensive understanding of the cellular electrophysiological mechanisms governing AVN function has remained elusive. This paper presents a detailed computational model of mouse AVN cell action potential (AP). Our model builds upon previous work and introduces several key refinements, including accurate representation of membrane currents and exchangers, calcium handling, cellular compartmentalization, dynamic update of intracellular ion concentrations, and calcium buffering. We recalibrated and validated the model against existing and unpublished experimental data. In control conditions, our model reproduces the AVN AP experimental features, (e.g. rate = 175 bpm, experimental range [121, 191] bpm). Notably, our study sheds light on the contribution of L-type calcium currents, through both Cav1.2 and Cav1.3 channels, in AVN cells. The model replicates several experimental observations, including the cessation of firing upon block of Cav1.3 or INa,r current. If block induces a reduction in beating rate of 11%. In summary, this work presents a comprehensive computational model of mouse AVN cell AP, offering a valuable tool for investigating pacemaking mechanisms and simulating the impact of ionic current blockades. By integrating calcium handling and refining formulation of ionic currents, our model advances understanding of this critical component of the cardiac conduction system, providing a platform for future developments in cardiac electrophysiology.
000145140 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000145140 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000145140 700__ $$aMesirca, Pietro
000145140 700__ $$aRicci, Eugenio
000145140 700__ $$aSales-Bellés, Clara$$uUniversidad de Zaragoza
000145140 700__ $$aTorre, Eleonora
000145140 700__ $$aLouradour, Julien
000145140 700__ $$aMangoni, Matteo Elia
000145140 700__ $$aSeveri, Stefano
000145140 7102_ $$15008$$2800$$aUniversidad de Zaragoza$$bDpto. Ingeniería Electrón.Com.$$cÁrea Teoría Señal y Comunicac.
000145140 773__ $$g602, 19 (2024), 4821-4847$$pJ. physiol.$$tJOURNAL OF PHYSIOLOGY-LONDON$$x0022-3751
000145140 8564_ $$s2947153$$uhttps://zaguan.unizar.es/record/145140/files/texto_completo.pdf$$yVersión publicada
000145140 8564_ $$s1885607$$uhttps://zaguan.unizar.es/record/145140/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000145140 909CO $$ooai:zaguan.unizar.es:145140$$particulos$$pdriver
000145140 951__ $$a2024-12-20-12:05:28
000145140 980__ $$aARTICLE