Sodium salicylate reduces inhibitory postsynaptic currents in neurons of rat auditory cortex

Effects of salicylate application on the spontaneous activity in brain slices of the mouse cochlear nucleus, medial geniculate body and primary auditory cortex

“…It could be hypothesized that the neurons without obvious changes in firing rate (or even with a decrease) are possibly inhibited from neurons which in turn were excited by salicylate. However, the different response types are also in accordance with results from patch-clamp recordings in AC and IC brain slices which showed a salicylate-induced depression of the delayed rectifier potassium current (Liu and Li, 2004a) and a reduction of inhibitory postsynaptic currents (Wang et al, 2006). Both effects could lead in turn to an increase of spontaneous activity while a blockage of voltage-gated sodium channels (Liu and Li, 2004b) should decrease the neuronal firing rate.…”

“…The results showed that the direct action of salicylate on central neurons is based on the depression of the delayed rectifier potassium current (Liu and Li, 2004a) and the blockage of voltage-gated sodium channels which shift the inactivation curve into the hyperpolarization range (Liu and Li, 2004b). It could also be demonstrated that salicylate reduces inhibitory postsynaptic currents in neurons of the auditory cortex (Wang et al, 2006).…”

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

“…Available evidence suggests that SS may produce tinnitus through directly targeting neurons and synapses in the central auditory system. Such lines of evidence include: (1) salicylate concentrations in the cerebrospinal fluid of animal models with behavioral manifestation of tinnitus induced by SS can reach a high level up to 1-2 mM (Deer and Hunter-Duvar, 1982;Jastreboff et al, 1986;Silverstein et al, 1967); (2) in a brain slice preparation, SS significantly reduces evoked inhibitory postsynaptic currents in rat auditory cortex (Wang et al, 2006) and changes the spontaneous activity of inferior colliculus neurons (Basta and Ernst, 2004); (3) treatment with SS injection increases the amplitude of local field potentials recorded from the auditory cortex of unanaesthetized rats (Yang et al, 2007) and changes spontaneous firing rate in the secondary auditory cortex of anesthetized cats (Eggermont and Kenmochi, 1998;Ochi and Eggermont, 1996); (4) animal microPET imaging shows that SS increases metabolic activity in the central auditory structures (Paul et al, 2007). These lines of evidence prompt a need to further explore how SS targets the central auditory system at a cellular and synaptic level in order to understand the exact neural mechanisms in SS-induced tinnitus.…”

Expression of Dopamine Receptor 1A and Cannabinoid Receptor 1 Genes in the Cochlea and Brain after Salicylate-Induced Tinnitus

“…For example, tinnitus was associated with increased activity or function of N-methyl- D -aspartate receptor (NR) in the inner ear [2], vanilloid receptor in the inner ear [3], acetylcholine receptor in the auditory cortex [4], and dopamine receptor (DR) in the auditolimbic dopaminergic pathway [5]. In contrast, decreased activity or function of cannabinoid receptor (CR) in the ventral cochlear nucleus [6] and γ-aminobutyric acid receptor (GABA receptor, GR) in the inferior colliculus (IC) [7] or auditory cortex [8] was found during the tinnitus condition. Recently, inflammation [9,10,11] and/or oxidative stress [12] were hypothesized as novel mechanisms for tinnitus.…”