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  • Altered neuronal intrinsic properties and reduced synaptic transmission of the rat's medial geniculate body in salicylate-induced tinnitus.

Altered neuronal intrinsic properties and reduced synaptic transmission of the rat's medial geniculate body in salicylate-induced tinnitus.

PloS one (2012-10-17)
Yan-Yan Su, Bin Luo, Yan Jin, Shu-Hui Wu, Edward Lobarinas, Richard J Salvi, Lin Chen
ABSTRACT

Sodium salicylate (NaSal), an aspirin metabolite, can cause tinnitus in animals and human subjects. To explore neural mechanisms underlying salicylate-induced tinnitus, we examined effects of NaSal on neural activities of the medial geniculate body (MGB), an auditory thalamic nucleus that provides the primary and immediate inputs to the auditory cortex, by using the whole-cell patch-clamp recording technique in MGB slices. Rats treated with NaSal (350 mg/kg) showed tinnitus-like behavior as revealed by the gap prepulse inhibition of acoustic startle (GPIAS) paradigm. NaSal (1.4 mM) decreased the membrane input resistance, hyperpolarized the resting membrane potential, suppressed current-evoked firing, changed the action potential, and depressed rebound depolarization in MGB neurons. NaSal also reduced the excitatory and inhibitory postsynaptic response in the MGB evoked by stimulating the brachium of the inferior colliculus. Our results demonstrate that NaSal alters neuronal intrinsic properties and reduces the synaptic transmission of the MGB, which may cause abnormal thalamic outputs to the auditory cortex and contribute to NaSal-induced tinnitus.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Sodium salicylate, puriss. p.a., ≥99.5% (NT)
Sigma-Aldrich
Sodium salicylate, tested according to Ph. Eur.
Sigma-Aldrich
Sodium salicylate, ReagentPlus®, ≥99.5%
Sigma-Aldrich
Sodium salicylate, meets USP testing specifications
Sigma-Aldrich
Sodium salicylate, puriss. p.a., reag. Ph. Eur., 99.5-101.0% (calc. to the dried substance)