Hearing loss caused by cochlear damage results in a variety of plastic changes in the central auditory pathways. One of these is hyperactivity, i.e. increased spontaneous firing rates, which may be involved in the generation of tinnitus, a phantom auditory sensation. The mechanism behind this synaptic plasticity is still uncertain but there may be a role for Brain Derived Neurotrophic Factor (BDNF). The expression of BDNF is activity dependent and BDNF can modulate synaptic plasticity leading to changes in excitability. In the present study we investigated the effects of two different types of cochlear trauma, mechanical and acoustic, at two different time points after trauma, on 1) peripheral hearing loss, 2) hyperactivity in inferior Colliculus (IC) and 3) BDNF protein expression in Cochlear Nucleus (CN) and IC of guinea pigs. BDNF protein expression was determined using ELISA. Although there was no significant difference in the amount of hearing loss between acoustic trauma and mechanical trauma animals, single neuron recordings showed higher levels of hyperactivity after mechanical trauma than after acoustic trauma at two weeks post-recovery from cochlear trauma.In addition, results showed an increase of BDNF levels in the ipsilateral CN and contralateral IC at 2 weeks after mechanical but not after acoustic trauma. BDNF levels recovered to sham control levels in both structures at 6 weeks after cochlear trauma even though hyperactivity remained higher compared to sham surgery animals at the same timepoint. The results suggest a possible time dependent role for BDNF in modulating synaptic plasticity and excitability after mechanical trauma to the cochlea.