Nociception, or the body’s ability to feel pain, is useful for survival as it tells humans to avoid situations that may cause them harm. Until now, it was believed that our pain sensors are equally receptive to all kinds of pain, but new research suggests our pain-sensing neurons are specialized for specific types of sensations.
In the interest of self-preservation, our brains and bodies are designed to help us avoid harmful or life-threatening situations.
Pain may be unpleasant, but its benefits become apparent in extreme clinical cases of people who lack the ability to feel pain. Such individuals may live with infections without being aware of them, self-mutilate, or generally have shortened life spans.
The neurons responsible for alerting us of potentially damaging stimuli are called nociceptors and are organized in a peripheral network that detects extreme temperatures, pressure, and injury-related chemicals.
New research sheds more light on how these pain sensors actually work.
Previous research used electrodes to examine pain-sensing neurons, but scientists have pointed out the limits of such testing models.
Pain cannot be monitored directly in animals, since they do not have the ability to verbalize their sensations. Pain in rodents has to be estimated by examining motor responses to stimuli.
However, the reactions monitored do not necessarily mean there is a simultaneous sensation of pain, and scientists need to identify the most relevant reactions to pain – such as paw licking or jumping – before performing experiments.
Researchers have also noted the challenges and limits of pain-testing models that rely on electrical stimulation.
Electrodes are an unnatural type of stimulation, and “electrical thresholds are rarely studied for themselves,” some authors have noted. This might compromise the research performed on rodents.
Researchers at University College London (UCL) in the United Kingdom think that the previous pain-assessment models based on electrodes were invasive and had altered the neurons’ properties.
This is why for their new study, the researchers used a kind of noninvasive, fluorescent activity-dependent imaging to study pain-sensing neurons in mice.
In the study – led by Dr. Edward Emery from UCL’s Wolfson Institute for Biomedical Research – the pain-receptive neurons were genetically marked to emit a fluorescent glow when activated.
The mice were either slightly pinched or exposed to cold and hot water stimuli on their paws to see which neurons were activated.
They discovered that over 85 percent of pain sensors react only to specific types of pain, while being unresponsive to others.
Dr. Emery thinks that previous research mistakenly showed that pain sensors are responsive to all kinds of pain, when in fact, they are quite selective in their response.
Previous research was compromised by the invasive electrode-based form of assessment, according to Dr. Emery.
“While the majority of neurons are specific to one type of pain, they can become universal pain sensors when the tissue is damaged. This may explain the discrepancies between our findings and those from other studies where more invasive approaches have been used.”
Dr. Edward Emery
The results of the study were recently published in the journal Science Advances.
“Our next step is to look at animal models for specific chronic pain conditions to see which neurons cells are activated,” says senior author John Wood, professor at UCL’s Wolfson Institute for Biomedical Research.
In the long run, the findings could improve the efficacy of painkillers. Scientists might be able to develop more specialized ones that target specific pain conditions more efficiently.
“We hope to identify the different neurons through which chronic pain can develop, so that focused treatments can be developed,” Wood adds. “We use ‘chronic pain’ to describe all sorts of pain conditions with different causes, but we now need to differentiate them so that we can develop new specific treatments.”