Differential effects of sodium salicylate on current-evoked firing of pyramidal neurons and fast-spiking interneurons in slices of rat auditory cortex

Sodium salicylate (SS) can penetrate the blood–brain barrier to target neurons in the central auditory system. Understanding how SS alters functional behaviors of different types of central auditory neurons will provide insights into the neural mechanisms of SS-induced tinnitus. Here, we report the differential effects of SS on current-evoked firing of pyramidal neurons and fast-spiking interneurons in layer II/III of auditory cortex slices in young rats (P12–P19). The two neuronal types were identified according to their characteristic patterns of current-evoked firing as recorded with whole-cell patch-clamp techniques and by their morphological features. Following perfusion of the brain slice with 1.4 mM SS, the threshold current needed to evoke an action potential remained unchanged for pyramidal neurons (68.96 ± 10.68 pA vs 70.39 ± 12.14 pA, n = 7, P > 0.05), but significantly increased for fast-spiking interneurons (56.9 ± 13.69 pA vs 74.04 ± 15.73 pA, n = 7, P < 0.05). The drug perfusion caused no significant change in current-evoked firing rates in pyramidal neurons (−2.43 ± 7.07%, n = 14, P > 0.05); however, it drastically and reversibly depressed those in fast-spiking interneurons by up to −49.88 ± 10.39% (n = 14, P < 0.05). Our results suggest that functionally impairing fast-spiking interneurons, which are GABAergic and inhibitory, is probably one of the pathways through which SS raises excitability in the central auditory system and consequently produces tinnitus.