Could the brain be tricked to perceive colours and sounds instead of pain?
Monday, 15 November, 2010
A group of Australian and Austrian researchers have located a key gene behind the body’s perception of pain, a mutation of which has been shown to replace pain with other sensations.
Known as synaesthesia, the condition sees the brain experiencing things that don’t typically occur in response to a given stimuli, for instance when music, words or numbers are perceived as colours.
Dr Greg Neely commenced his research at the Austrian Academy of Sciences in Vienna, where he collaborated with Professor Josef Penninger, head of the academy. Neely is now continuing his work at Sydney’s Garvan Institute of Medical Research, which he recently joined as a researcher.
Neely's team first screened the genome of fruit flies to examine perception of pain, especially the insect’s response to heat-induced pain. This gave them a pool of 600 genes related to pain perception, from which they isolated one, the so-called α2δ3 gene.
Shared by both mice and humans, the researchers observed that α2δ3 appeared to trigger the same cellular reactions as certain painkillers.
Collaborators from US universities Harvard, Pittsburgh and North Carolina then set about examining variations in the gene within humans.
One of the variations they found not only reduced sensitivity to acute pain, but it also made people less vulnerable to chronic lower back pain. Subsequent MRI scans of mice with this particular mutation revealed that the gene plays a key role in the brain’s perception of heat-related pain.
With these mice, the pain impulse first arrives where it’s supposed to; at the part of the brain called the thalamus, the brain’s initial processing centre. But the genetic mutation sees it losing its way from there, and instead of travelling to the higher processing centres responsible for alerting animals to the sensation of pain, perversely it triggers those parts of the brain responsible for sight, smell and hearing.
“From a medical research perspective, our findings help explain the wide variance in how people experience pain,” said Dr Neely.
“Not only that, they indicate potential ways of treating acute and chronic pain in the future – by mimicking the effects of the mutated gene.”
He added that the research is especially significant for neuroscientists, as it provides the first known genetic insights into the mechanisms behind synaesthesia.
For instance, MRI scans of mice with the mutated gene showed that the parts of their brains associated with smell, sound and vision were stimulated when they were exposed to heat.
“If you think of the neurons in the brain as wires with insulation, it’s as if their sensory insulation had been stripped, and a trigger to one sensory input, like touch or heat, could be perceived as another,” Dr Neely explained.
“In these mice, a part of the brain often referred to as the ‘pain matrix’ didn’t light up as much as normal because the pain signals were unable to spread to these higher structures in the brain.”
Furthermore, the researchers also reported that when they touched the whiskers of affected mice, it appeared as though they could hear, smell and see touch.
The findings could one day lead to applications that are able to translate pain into other less troubling sensations such as the sounds of music or sense of colours.
The study appears in the current issue of Cell.
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