Functional and morphological differences between temporary (TTS) and permanent (PTS) hearing loss induced by acoustic trauma are well characterized whereas molecular differences remain to be elucidated. A comparative analysis of the expression of the phosphorylated forms of extracellular signal-regulated kinase (ERK1/2), c-jun-N-terminal kinases 1/2 (JNK1/2) and p38 in the mouse cochlea after acoustic trauma resulting in either a temporary or permanent damage is presented. In the acute phase of PTS an upregulation of phosphorylated p38, JNK1/2, and ERK1/2 was found while in the acute phase of TTS a downregulation of phospho-p38 occurred and no immediate change of pJNK1/2 and pERK1/2 was noted. After a 24 h recovery from TTS JNK1/2 and ERK1/2 was activated while the expression of phospho-p38 was downregulated. In contrast PTS group showed complete recovery to control values for all three MAPKs by 24 h post. The level of brain-derived neurotrophic factor (BDNF), a potent otoprotective agent, was elevated after both types of acoustic trauma but the elevation after permanent trauma was of a longer duration. The expression of BDNF receptor's TrkB (truncated form) was downregulated only after permanent hearing loss. Thus, temporary and permanent hearing loss demonstrate different expression patterns and temporal aspects of MAPK, BDNF and TrkB in the cochlea. The results of this study will help reveal the cellular mechanisms underlying hearing loss induced by acoustic trauma.