| First Author | Calton MA | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 5 | Pages | e94549 |
| PubMed ID | 24804771 | Mgi Jnum | J:216087 |
| Mgi Id | MGI:5607685 | Doi | 10.1371/journal.pone.0094549 |
| Citation | Calton MA, et al. (2014) A lack of immune system genes causes loss in high frequency hearing but does not disrupt cochlear synapse maturation in mice. PLoS One 9(5):e94549 |
| abstractText | Early cochlear development is marked by an exuberant outgrowth of neurites that innervate multiple targets. The establishment of mature cochlear neural circuits is, however, dependent on the pruning of inappropriate axons and synaptic connections. Such refinement also occurs in the central nervous system (CNS), and recently, genes ordinarily associated with immune and inflammatory processes have been shown to play roles in synaptic pruning in the brain. These molecules include the major histocompatibility complex class I (MHCI) genes, H2-K(b) and H2-D(b), and the complement cascade gene, C1qa. Since the mechanisms involved in synaptic refinement in the cochlea are not well understood, we investigated whether these immune system genes may be involved in this process and whether they are required for normal hearing function. Here we report that these genes are not necessary for normal synapse formation and refinement in the mouse cochlea. We further demonstrate that C1qa expression is not necessary for normal hearing in mice but the lack of expression of H2-K(b) and H2-D(b) causes hearing impairment. These data underscore the importance of the highly polymorphic family of MHCI genes in hearing in mice and also suggest that factors and mechanisms regulating synaptic refinement in the cochlea may be distinct from those in the CNS. |
