Inflammation in a sound-processing region of the brain mediates ringing in the ears in mice that have noise-induced hearing loss, according to a study publishing June 18 in the open-access journal PLOS Biology by Shaowen Bao of the University of Arizona, and colleagues.
Hearing loss is a widespread condition that affects approximately 500 million individuals, and is a major risk factor for tinnitus -- the perception of noise or ringing in the ears. Recent studies indicate that hearing loss causes inflammation -- the immune system's response to injury and infection -- in the auditory pathway. But its contribution to hearing loss-related conditions such as tinnitus is still poorly understood. To address this gap in knowledge, Bao and his colleagues examined neuroinflammation -- inflammation that affects the nervous system -- in the auditory cortex of the brain following noise-induced hearing loss, and its role in tinnitus, in rodent models.
The results indicate that noise-induced hearing loss is associated with elevated levels of molecules called proinflammatory cytokines and the activation of non-neuronal cells called microglia -- two defining features of neuroinflammatory responses--in the primary auditory cortex. Experiments in mice that incur noise-induced hearing loss showed that a cell-signaling molecule called tumor necrosis factor alpha (TNF-α) mediates neuroinflammation, tinnitus, and synaptic imbalance -- an altered pattern of signaling between neurons. Moreover, the researchers found that pharmacological blockade of TNF-α or depletion of microglia prevented tinnitus in mice with noise-induced hearing loss. According to the authors, the findings suggest that neuroinflammation may be a therapeutic target for treating tinnitus and other hearing loss-related disorders.