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Injury to areas of the central nervous system can alter neurotrophin levels, which may influence postlesion neuronal survival and plasticity. To determine if sensorineural hearing loss induces such changes, we used an enzyme-linked immunosorbent assay (ELISA) to measure neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF) levels in adult guinea pig brain stem auditory nuclei 3-60 days after a unilateral cochlear ablation (UCA). After UCA, which destroyed the cochlea and cochlear nerve on one side, NT-3 levels were usually depressed at 3 days by 22-44% but became elevated transiently at 7 days by 28-124%. BDNF levels were elevated transiently by 50% on the ablated side in the anteroventral (AVCN) and posteroventral (PVCN) cochlear nucleus at 3 days and may have signaled support for the survival of deafferented neurons. Coincident elevation at 3 and 7 days of BDNF or NT-3 and phosphorylated extracellular signal-regulated protein kinase 2 (ERK2-P) suggested a relationship to stimulated signal transduction activity. Elevated neurotrophin levels may have contributed to synaptogenesis in the AVCN and the superior olive and to changes in the synaptic biochemistry in the auditory nuclei after UCA. In contrast, deficiencies or failure to elevate neurotrophin levels within several days of the UCA correlated with upregulation of phosphorylated stress-activated protein kinase (SAPK-P), suggesting a relationship with stress-activated signal transduction and with the sparse degeneration of fibers observed in some of the auditory nuclei after UCA.