Mechanism behind Development of Tinnitus following Exposure to Loud Sounds Identified
Exposure to loud noises often leads to development of tinnitus, a condition wherein the patient experiences a ringing sensation in the ear even in the absence of any external sound. 10% people are said to be affected by the condition and it has been postulated that it results from damage to nerve cells in the ears. At present, there is no treatment available to prevent the development of tinnitus or to treat it. However, in an important breakthrough, researchers from the University of Leicester's Department of Cell Physiology and Pharmacology have identified the mechanism behind the development of tinnitus following exposure to loud sound. The understanding of this mechanism could pave way for the development of medicines that could prevent or treat this condition.
The results of the study, which was carried out under the leadership of Dr. Martine Hamann, have been published in the latest issue of the journal Hearing Research. The researchers specifically looked at the behavior of the fusiform cells present in the dorsal cochlear nucleus in the brain, an area which receives signals from nerve cells in the ear and transmits it to other parts of the brain for decoding. They observed that these fusiform cells exhibit increased cellular excitability following acoustic over-exposure (AOE) and start firing erratically. This may result in tinnitus.
The researchers were also able to identify the key cellular mechanisms which lead to increased excitability of these fusiform cells in the dorsal cochlear nucleus. According to them, this is a result of malfunctioning of specific potassium channels which, in turn, prevent the cells from coming back to their resting state. They, therefore, continue to fire erratically which leads the patient to hear sounds even in the absence of any auditory stimuli. According to the researchers, targeting these specific potassium channels and preventing their malfunctioning, can lead to prevention of tinnitus.
Thursday, October 2, 2014