Spontaneous hyperactivity in the dorsal cochlear nucleus (DCN), particularly in fusiform cells, has been proposed as a neural generator of tinnitus. To determine if sodium salicylate, a reliable tinnitus inducer, could evoke hyperactivity in the DCN, we measured the spontaneous and depolarization-evoked spike rate in fusiform and cartwheel cells during salicylate superfusion. Five minute treatment with 1.4 mM salicylate suppressed spontaneous and evoked firing in fusiform cells; this decrease partially recovered after salicylate washout. Less suppression and greater recovery occurred with 3 min treatment using 1.4 mM salicylate. In contrast, salicylate had no effect on the spontaneous or evoked firing of cartwheel cells indicating that salicylate's suppressive effects are specific to fusiform cells. To determine if salicylate's suppressive effects were a consequence of increased synaptic inhibition, spontaneous inhibitory postsynaptic currents (IPSC) were measured during salicylate treatment. Salicylate unexpectedly reduced IPSC thereby ruling out increased inhibition as a mechanism to explain the depressed firing rates in fusiform cells. The salicylate-induced suppression of fusiform spike rate apparently arises from unidentified changes in the cell's intrinsic excitability.
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