This paper reviews efforts to determine if a unilateral hearing loss altered inhibitory glycinergic synapses in the cochlear nucleus (CN) and the superior olive. In young adult guinea pigs, 2-147 days after unilateral cochlear ablation, we quantified the electrically evoked release and the high-affinity uptake of [(14)C]glycine as measures of transmitter release from glycinergic presynaptic endings and glycine removal from extracellular spaces. The specific binding of [(3)H]strychnine was quantified to measure synaptic glycine receptor activity and/or expression. Three types of post-lesion change were observed. First, several tissues exhibited changes consistent with a persistent deficiency in glycinergic inhibitory transmission. Deficient binding prevailed on the ablated side in the anterior and caudal anteroventral CN, the posteroventral CN and the lateral superior olive (LSO), while glycine release was near normal and uptake was elevated (except in the LSO). However, deficient release prevailed in the dorsal CN, bilaterally, and was accompanied by elevated uptake. Second, the LSO on the intact side exhibited changes consistent with strengthened glycinergic inhibition, as binding was elevated while release and uptake were near normal. Third, several tissues exhibited various transient changes in activity. These types of post-lesion change might contribute to altered auditory functions, which often accompany hearing loss.