Characterization of EGR-1 Expression in the Auditory Cortex Following Kanamycin-Induced Hearing Loss in Mice.

Deprivation of acoustic input during a critical period leads to abnormal auditory development in humans. The molecular basis underlying the susceptibility of auditory cortex to loss of afferent input remains largely unknown. The transcription factor early growth response-1 (EGR-1) expression in the visual cortex has been shown to be crucial in the formation of vision, but the role of EGR-1 during the process of auditory function formation is still unclear. In this study, we presented data showing that EGR-1 was expressed in the neurons of the primary auditory cortex (A1) in mice. We observed that the auditory deprivation induced by kanamycin during the auditory critical period leads to laminar-specific alteration of neuronal distribution and EGR-1 expression in A1. In addition, MK-801 administration inhibited the expression of EGR-1 in A1 and aggravated the abnormal cortical electric response caused by kanamycin injection. Finally, we showed that the expression of PI3K, the phosphorylation of Akt, as well as the phosphorylation of cAMP-responsive element-binding protein (CREB) were decreased in A1 after kanamycin-induced hearing loss. These results characterized the expression of EGR-1 in A1 in response to the acoustic input and suggested the involvement of EGR-1 in auditory function formation.