Sodium salicylate suppresses serotonin-induced enhancement of GABAergic spontaneous inhibitory postsynaptic currents in rat inferior colliculus in vitro.

Available evidence suggests that sodium salicylate (SS) may produce tinnitus through altering the balance between inhibition and excitation in the central auditory system. Since serotonin (5-hydroxytryptamine, 5-HT) containing fibers preferentially innervate inhibitory GABA neurons, there exists a possibility that SS causes the imbalance between inhibition and excitation through influencing serotonergic modulation of the GABAergic synaptic transmission. In the present study, we examined the effects of SS on 5-HT-mediated GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) from neurons of the central nucleus of rat inferior colliculus with whole-cell patch-clamp technique and brain slice preparation. Perfusion of 40 microM 5-HT robustly enhanced both frequency and amplitude of GABAergic sIPSCs and this 5-HT-induced enhancement of GABAergic sIPSCs could be suppressed by 1.4mM SS. Tetrodotoxin at 0.5 microM produced a similar effect as SS did, suggesting that SS suppresses the 5-HT-induced enhancement of GABAergic sIPSCs through depressing spontaneous action potentials of GABA neurons. Our findings suggest that SS may preferentially target GABA neurons and consequently interrupt a normal level of GABAergic synaptic transmissions maintained by the serotonergic system in SS-induced tinnitus.