S-067
Rol of medial olivocochlear efferent activity in central auditory synapse development.
Daniela Maria Chequer Charan1, Wenqing Huang2, María Eugenia Gómez-Casati3, Yunfeng Hua2, Ana Belén Elgoyhen1, Mariano Nicolas Di Guilmi1
  1. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular “Dr. Héctor N. Torres” (INGEBI), Laboratorio de Fisiología y Genética de la Audición, Buenos Aires, Argentina
  2. Shanghai Jiao Tong University School of Medicine, Ninth People’s Hospital, Shanghai Institute of Precision Medicine, Shanghai, China
  3. Instituto de Farmacología, Facultad de Medicina. Universidad de Buenos Aires. Argentina
Presenting Author:
Daniela Maria Chequer Charan
danichch92@gmail.com
At birth, the auditory system of most mammals is functionally immature and requires a postnatal period of synaptic refinement to achieve the precise connectivity observed in adulthood. During this developmental window, the medial olivocochlear (MOC) efferent system modulates spontaneous inner ear activity, thereby affecting the maturation of central circuits. In mice with enhanced MOC activity (α9KI), synaptic dysfunction was found at the calyx of Held (CH) within the medial nucleus of the trapezoid body (MNTB) (Di Guilmi et al., 2019). In this study, we combined in vitro electrophysiology (P12–14) with 3D morphological reconstructions (P12–14 and P21–25) using serial electron microscopy in three genotypes: wild type (WT), α9KI, and α9KO (lacking MOC activity) and a custom Python-based code to extract quantitative parameters, enabling the classification of CHs into distinct morphotypes. Recordings in the α9KI mice displayed synaptic alterations across several parameters, evidenced by a lower excitatory post-synaptic current, a higher short-term depression and smaller ready realizable vesicle pool. Morphological analyses revealed a lower proportion of structurally complex CHs and decreased synaptic pruning in α9KI animals. By contrast, α9KO only showed reduced morphological complexity. These results suggest that enhanced MOC activity drives more profound developmental modifications in MNTB circuitry compared to the absence of MOC modulation.