Washington: A new study provides compelling evidence to suggest that insects also experience chronic pain, which persists long after the healing of an initial injury.
The study published in the journal Science Advances offers the first genetic evidence of the cause of chronic pain in Drosophila (fruit flies) with good evidence that similar changes also drive chronic pain in humans.
Ongoing research into these mechanisms could lead to the development of treatments that, for the first time, target the cause and not just the symptoms of chronic pain.
“If we can develop drugs or new stem cell therapies that can target and repair the underlying cause, instead of the symptoms, this might help a lot of people,” said Associate Professor Neely, whose team of researchers is studying pain with the goal of developing non-opioid solutions for pain management.
“People don’t really think of insects as feeling any kind of pain. But it’s already been shown in lots of different invertebrate animals that they can sense and avoid dangerous stimuli that we perceive as painful. In non-humans, we call this sense ‘nociception’, the sense that detects potentially harmful stimuli like heat, cold, or physical injury, but for simplicity, we can refer to what insects experience as ‘pain’,” said Associate Professor Neely.
“So we knew that insects could sense ‘pain’, but what we didn’t know is that an injury could lead to long-lasting hypersensitivity to normally non-painful stimuli in a similar way to human patients’ experiences.”
The study of fruit flies looked at neuropathic ‘pain’, which occurs after damage to the nervous system and, in humans, is usually described as a burning or shooting pain.
Neuropathic pain can occur in human conditions such as sciatica, a pinched nerve, spinal cord injuries, postherpetic neuralgia (shingles), diabetic neuropathy, cancer bone pain, and in accidental injuries.
In the study, Associate Professor Neely and lead author Dr Thang Khuong damaged a nerve in one leg of the fly. The injury was then allowed to fully heal. After the injury healed, they found the fly’s other legs had become hypersensitive.
“After the animal is hurt once badly, they are hypersensitive and try to protect themselves for the rest of their lives. That’s kind of cool and intuitive,” said Associate Professor Neely.
Next, the team genetically dissected exactly how that works.
“The fly is receiving ‘pain’ messages from its body that then go through sensory neurons to the ventral nerve cord, the fly’s version of our spinal cord. In this nerve cord are inhibitory neurons that act like a ‘gate’ to allow or block pain perception based on the context. After the injury, the injured nerve dumps all its cargo in the nerve cord and kills all the brakes, forever.
Then the rest of the animal doesn’t have brakes on its ‘pain’. The ‘pain’ threshold changes and now they are hypervigilant,” Associate Professor Neely said.
“In humans, chronic pain is presumed to develop through either peripheral sensitisation or central disinhibition. From our unbiased genomic dissection of neuropathic ‘pain’ in the fly, all our data points to central disinhibition as the critical and underlying cause for chronic neuropathic pain,” the professor said.