Neural excitability, synaptic transmission and neuron-glia interactions
Author: Camila Catalano Di Meo | Email: ccatalano98@gmail.com
Camila Catalano Di Meo1°2°, Valeria Castagna2°, Marcelo Moglie1°, Jimena Ballestero2°, María Eugenia Gomez-Casati2°, Juan Diego Goutman1°
1° Instituto de Ingeniería Genética y Biología Molecular, CONICET
2° Instituto de Farmacología, FMED-UBA
Intracellular Ca2+ compartmentalization is essential for cellular function and the maintenance of independent signaling pathways. Outer hair cells (OHCs) in the cochlea are responsible for the amplification of sound waves within the inner ear, crucial for fine sound detection. An important aspect of these cells is the precise regulation of Ca2+ homeostasis during their normal functioning. Ca2+ is thought to be involved in mechanotransduction -the process by which these cells detect sound signals- and in synaptic communication between OHCs and neurons projecting to and from the inner ear. Common causes of hearing loss are Ca2+ excitotoxicity in OHCs following noise over-exposure. Recent transcriptomic studies have identified two highly expressed genes related to intracellular Ca2+ homeostasis in OHCs: oncomodulin and sorcin. Whereas the former is a well described Ca2+ buffer, no clear role has been established in the cochlea for the latter. Sorcin is crucial in regulating the Ca2+ cycle and the excitation-contraction coupling in cardiac muscle. It has been demonstrated that sorcin can modulate the phenomenon of “Ca2+ induced Ca2+ release” by binding to, and regulating, various essential Ca2+ homeostasis proteins such as ryanodine receptors, L-type Ca2+ channels, and SERCA pumps. This study aims to determine the role of sorcin in the regulation and dynamics of Ca2+ in mouse cochlear OHCs, based on the hypothesis that high sorcin expression in OHCs is crucial for Ca2+ regulation