Intoxication by sodium salicylate induces tinnitus in both humans and experimental animals. Tinnitus, in most cases, is caused by central mechanisms leading to hyperactivity of some central auditory regions, in special the fusiform neurons of the dorsal cochlear nucleus (DCN) in the brainstem. One hypothesis for the origin of hyperactivity is an unbalance of the inhibitory and excitatory neurotransmission in auditory areas. Salicylate inhibits the enzyme cyclooxygenase 2 which takes part in the oxidative degradation of endocannabinoids. Here we are testing the hypothesis that salycilate interferes with endocannabinoid mediated synaptic plasticity in the DCN. For this we tested the effect of sodium salicylate on the phenomenon of depolarization suppression of excitation (DSE) in parallel fibers (PF) synapses on glutamatergic fusiform and glycinergic cartwheel neurons of the DCN, which is mediated by endocannabinoids. Brain slices were prepared from 18 to 22 days old Wistar rats, and glutamatergic neurotransmission was elicited by stimulating the (PF) with a bipolar electrode, in the presence of picrotoxin and strychnine to block inhibitory neurotransmission. Post-synaptic currents were recorded at -80 mV in whole-cell voltage clamp. DSE was produced by a depolarization to 0 mV with duration of 0.5, 1, 2 and 4 seconds. As reported in mice DSE was stronger in cartwheel than in fusiform neurons (maximum DSE at 4 seconds: cartwheel 41 ± 5%; fusiform 21 ± 5%. N = 19 and 12 respectively. P = 0.0002, 2-way ANOVA). Incubation of the slices with sodium salicylate (NaSal, 1.4 mM) for at least 1 hour before the recording did not affect the PF-evoked EPSC amplitude either in cartwheel (control: -414 ± 60 pA; NaSal: -756 ± 207 pA; n=12 and 18 respectively, p=0.08, t-test) and fusiform neurons (control: -454 ± 104 pA; NaSal: -404 ± 66 pA; n=8 and 10 respectively. p=0.68, t-test). However, salicylate enhanced the DSE in cartwheel neurons significantly (p<0.05, 2-way ANOVA; n=9) but not in fusiform neurons. Maximum DSE after 4 seconds depolarization in cartwheel neurons was not affected by salicylate, but was attained earlier after 2 seconds depolarization (control 26 ± 5 %; NaSal: 43 ± 7%; p = 0.05, t-test). Acute applications of salicylate produced similar changes in the DSE profile of cartwheel neurons but again did not affect DSE in fusiform neurons. We conclude that sodium salicylate in concentrations similar to found in the cerebrospinal fluid after tinnitus-inducing salicylate intoxication is able to enhance DSE in DCN’s cartwheel neurons. Since cartwheel neurons produces feed forward inhibition onto fusiform neurons, an increased DSE can weakens inhibition during high frequency trains of firing from the PF and can contribute for generating hyperactivity in the fusiform neurons after salicylate intoxication.