Upregulation of insulin-like growth factor and interleukin 1β occurs in neurons but not in glial cells in the cochlear nucleus following cochlear ablation.

One of the main mechanisms used by neurons and glial cells to promote repair following brain injury is to upregulate activity-dependent molecules such as insulin-like growth factor 1 (IGF-1) and interleukin-1β (IL-1β). In the auditory system, IGF-1 is crucial for restoring synaptic transmission following hearing loss; however, whether IL-1β is also involved in this process is unknown. In this study, we evaluated the expression of IGF-1 and IL-1β within neurons and glial cells of the ventral cochlear nucleus in adult rats at 1, 7, 15, and 30 days following bilateral cochlear ablation. After the lesion, significant increases in both the overall mean gray levels of IGF-1 immunostaining and the mean gray levels within cells of the cochlear nucleus were observed at 1, 7, and 15 days compared with control animals. The expression and distribution of IL-1β in the ventral cochlear nucleus of ablated animals was temporally and spatially correlated with IGF-1. We also observed a lack of colocalization between IGF-1 and IL-1β with either astrocytes or microglia at any of the time points following ablation. These results suggest that the upregulation of IGF-1 and IL-1β levels within neurons-but not within glial cells-may reflect a plastic mechanism involved in repairing synaptic homeostasis of the overall cellular environment of the cochlear nucleus following bilateral cochlear ablation.