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Krishnan AV, Trump DL, Johnson CS, Feldman D

In: Czuczwar SJ, editor

Their beneficial mechanisms can include the attenuation of neuroinflammation [e.g., valproate via histone deacetylase (HDAC) inhibition in microglia, downregulating interleukin-1 beta (IL-1) and inducible nitric oxide synthase (iNOS)] or the mitigation of glutamatergic excitotoxicity coupled with enhancement of neurotrophic factor expression (e.g., lamotrigine), thereby conferring antidepressant-like potential (Mula and Sander, 2007

This hyperactivity subsequently propagates through the inferior colliculus to the auditory thalamus, and ultimately to the primary auditory cortex