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


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Abstract

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 μM 5-HT robustly enhanced both frequency and amplitude of GABAergic sIPSCs and this 5-HT-induced enhancement of GABAergic sIPSCs could be suppressed by 1.4 mM SS. Tetrodotoxin at 0.5 μM 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.

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