Please make it stop

Residual synaptic endings may cause the horrid cacophony
sufferers of tinnitus hear. Chinchillas too should
stay away from jet engines

By Brian Hoyle

The buzzing, ringing, booming, and many other sounds that constitute tinnitus can develop at any age in anyone. For over 360,000 Canadians, tinnitus is "annoying," while life for 150,000 others is seriously impaired, according to the Tinnitus Association of Canada.

Dr Steven Potashner has a personal stake in tinnitus. It affects members of his family and his frustration in obtaining effective treatment for them spurred the professor of neuroscience at the University of Connecticut Health Center in Farmington, to action. The results of a study headed by Dr Potashner appear in the February 15 issue of the Journal of Neuroscience Research.

He and his colleagues hypothesized that adult exposure to loud noise could damage the cochlea, its nerve axons, and their synaptic endings in the brain.

The hypothesis was tested on chinchillas. Unlike other rodents, a chinchilla's hearing is very similar to that of humans. "Their cochleas are as sensitive to noise damage as human cochleas," says Dr Potashner. "Since tinnitus often results from hearing loss, the chinchilla with a noise-damaged cochlea seemed a good model."

In the experiments, anesthetized chinchillas had one ear plugged with silicone and were exposed to a jet engine blast of 108 decibels. As predicted, the cochlea of the unplugged ear did not come through the sound assault unscathed. Degeneration of the cochlear nerve fibres and their synaptic brain connections, and damage to the cochlear hair cells that respond to the various sound frequencies, were observed within 14 days of the sonic blast.

During the first week after the sonic challenge, before the nerve axons began to degenerate, the release of the neurotransmitter glutamate was more pronounced. Subsequently, the release declined as nerve fibre degeneration occurred. At 90 days, neurotransmitter release and the number of glutamate receptors rebounded in some areas of the cochlear nucleus in the brain. The plugged ear was not damaged in any way.

"After the cochlear nerves have died, the residual synaptic endings... have either somehow increased their capacity to release the transmitter, or new synaptic endings have grown and are participating in the release at normal capacity," says Dr Potashner. The new synaptic contacts... may occupy the sites left vacant by the degenerated nerve fibres that funnelled information from the cochlea. The researchers feel that these new fibres might excite the cochlear nucleus in the absence of any real stimulating sound resulting in tinnitus. Work continues to identify other "potential therapeutic targets."