Molecular Plasticity in the Rat Auditory Brainstem: Modulation of Expression and Distribution of Phosphoserine, Phospho-CREB and TrkB after Noise Trauma

Abstract

We induced acoustic trauma by applying click stimuli of 130 dB (SPL) for 30 min to one ear of adult rats. This treatment resulted in an instant and permanent threshold shift of 96 dB in the affected ear. A massive reduction of cochlear nerve fibers in the ventral cochlear nucleus (VCN) was demonstrated by tracing them from the cochlea of rats that survived acoustic overstimulation for 1 year or longer. In the auditory brainstem, we observed a deprivation-dependent appearance of fibers positive for tyrosine receptor kinase B in the ipsilateral VCN between day 3 and day 21 after trauma and an increase in phosphoserine immunostaining in the neuropil of the ipsilateral VCN and in neurons of the contralateral lateral superior olive during the first 30 days after trauma. Immunoreactivity for the cAMP response element binding protein in its phosphorylated form was transiently depressed in the ipsilateral inferior colliculus immediately after trauma and was elevated as late as 7 months after trauma in the ipsilateral VCN. Apparently, a unilateral acoustic overstimulation entails specific regulations of the activity of plasticity-associated molecules through phosphorylation and includes changes to neurotrophin signaling between neurons of the auditory brainstem.