Hyperacusis
Hearing Health Foundation’s Emerging Research Grants (ERG) program awards grants to researchers studying hyperacusis including:
Mechanisms of hyperacusis
Development of animal models
Genetics of hyperacusis
Etiology, diagnosis, and treatment of hyperacusis
Brain imaging, biomarkers, electrophysiology of hyperacusis
Distinctions between hyperacusis and tinnitus
Interaction between auditory nerve and trigeminal nerve information
ERG awards are for up to $50,000 per year, one year in length in the first instance, and renewable for a second year. Find more information below about hyperacusis projects awarded a grant in prior years.
University of Pittsburgh
KCNQ2/3 potassium channel activator mitigates noise-trauma–induced hypersensitivity to sounds
in mice
Noise-induced hearing loss (NIHL) is one of the most common causes of hearing disorders. NIHL reduces the auditory sensory information relayed from the cochlea to the brain, including the primary auditory cortex (A1). To compensate for reduced peripheral sensory input, A1 undergoes homeostatic plasticity. Namely, the sound-evoked activity of A1 excitatory principal neurons (PNs) recovers or even surpasses pre-noise trauma levels and exhibits increased response gain (the slope of neuronal responses against sound levels). This increased gain of A1 PNs after NIHL is associated with highly debilitating hearing disorders, such as tinnitus (perception of phantom sounds), hyperacusis (painful perception of sounds), and hypersensitivity to sounds (increased sensitivity to everyday sounds). Despite the high prevalence of these hearing disorders, treatment options are limited to cognitive behavioral therapy and hearing prosthetics with no FDA-approved pharmacotherapeutic options available. Therefore, to aid in the development of pharmacotherapeutic options, it is imperative to 1) develop animal models of these hearing disorders, 2) identify the brain plasticity underlying these hearing disorders, and 3) test potential pharmacotherapy to rehabilitate hearing and brain plasticity after NIHL. Here, we aim to develop a novel mouse model of hypersensitivity to sounds, identify its underlying A1 plasticity, and test pharmacotherapy to mitigate it after NIHL.