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Previous studies suggest that sodium salicylate (NaSal), an asparin metabolite, raises the neural excitability in the auditory cortex to cause tinnitus.In the present study, we wanted to determine whether NaSal had a similar effect in the medial geniculate body (MGB), a central auditory structure that provides the immediate inputs to the auditory cortex.Using whole-cell patch-clamp recordings from MGB slices in rats, we measured effects of NaSal (1.4 mmol/L) on neuronal intrinsic properties and the synaptic transmission.We found that NaSal decreased the membrane input resistance, hyperpolarized the resting membrane potential, suppressed the current-evoked firing, changed action potential properties and depressed rebound depolarization.NaSal also reduced the postsynaptic response evoked by stimulating the brachium of inferior colliculus (BIC), indicating a reduction in efficacy of the synaptic transmission.Our results demonstrate that NaSal lowers the neural excitability via altering neuronal intrinsic properties and reducing the synaptic transmission in the MGB, which is distinct from its excitatory effects on the auditory cortex.We suggest that NaSal-induced tinnitus may be partly due to the abnormal neural synchrony in the auditory cortex resulting from the reduced excitability of the MGB.