The Pittsburgh Hearing Research Center recently had a paper published in Nature Communications highlighting a breakthrough.
Entitled “Cell-type-specific plasticity of inhibitory interneurons in the rehabilitation of auditory cortex after peripheral damage,” the article focuses on noise induced hearing loss.
Given the increasing environmental noise pollution in modern societies, exposure to loud sounds is an ever-growing public health problem, explained Manoj Kumar, PhD, one of the authors. Approximately 40 million adults in the U.S. have symptoms of noise induced hearing loss (NIHL). NILH is the leading cause of highly prevalent disorders like tinnitus and hyperacusis, with an overall economic impact of $150 billion within the U.S.
“Because of the growing number of individuals with NIHL and hearing loss-related disorders, the need to advance the development of treatment options is imperative and vastly dependent on understanding the circuit, synaptic, and intrinsic mechanisms of central plasticity after NIHL,” Dr. Kumar said.
In the study, the cell-type specific plasticity among different subtypes of inhibitory neurons in the mouse auditory cortex after NIHL were identified.
“Our results create a new framework for understanding the cellular and circuit mechanisms underlying brain plasticity after hearing loss and hold the promise to advance understanding of the cortical mechanisms underlying disorders associated with maladaptive cortical plasticity after peripheral damage, such as tinnitus, hyperacusis, visual hallucinations, and phantom limb pain,” Dr. Kumar said.
Additionally, “by knowing what each neuron does, we can further improve recovery (see also problems in perceiving sounds in noise) and also mitigate plasticity-related disorders,” added Thanos Tzounopoulos, PhD, Director of the Pittsburgh Hearing Research Center and another author on the study.