An incredible new study from scientists at Stanford University has homed in on a bundle of brain cells that seem to be responsible for the negative emotional experience associated with pain, as opposed to the physical sensation itself. This breakthrough insight into how pain is processed in the brain could lead to novel non-opioid treatments for chronic pain that eliminate the unpleasant feeling accompanying pain without removing the physical sensation.
"There's really no good treatment for chronic pain in humans, and that's a major driver of the opioid epidemic," says Gregory Scherrer, one of the Stanford researchers working on the project. "But you'll notice, patients who take opioids for pain report that they can still feel the sensation of pain but say it's less bothersome – the emotions of pain are different."
A great deal of modern pain research has concentrated on understanding how our body directly senses painful sensations from a nervous system perspective. When nerves in the hand detect it has been cut, for example, messages are sent to the brain communicating this sensation. Unfortunately, simply disrupting this nervous system pain signal is not the most realistic treatment idea. Acute pain signaling is important – it helps us avoid physical threats, and if it was blocked completely it would potentially lead to disastrous physical consequences.
"While painful stimuli are detected by nerves, this information doesn't mean anything emotionally until it reaches the brain," explains Scherrer, "so we set out to find the cells in the brain that are behind the unpleasantness of pain."
The research began by focusing on the amygdala, a part of the brain known to regulate emotion. Utilizing a novel visualization system to observe brain activity in mice, the study homed in on a specific brain region called the basolateral amygdala (BLA). Bundles of neurons in this region of the brain were seen to activate when the animals touched uncomfortably hot or cold water.
Interestingly, the researchers discovered that these BLA neurons did not activate when the animals were subjected to merely annoying physical disturbances, such as bad smells or puffs of air to the face. This affirmed that this bundle of BLA neurons was specifically firing in response to pain sensations.
The final stage of the research involved observing what happened when an experimental mouse model had its BLA neurons blocked from activating. A test was set up where a single walking track was split into three lanes. The middle lane was kept at a comfortable temperature, with the left side presenting as uncomfortably cold and the right as hot. These temperatures were not physically damaging, but rather unpleasant in the same way walking barefoot on a sidewalk in extreme summer or winter conditions would be uncomfortable.
The BLA-blocked mice notably moved around the extreme fringes of the walking track, seemingly unbothered by the extreme temperatures. An exposure test, dropping hot water on the animal's paw, revealed the experimental mice withdrawing quickly, but also returning its paw back to its original position, something a normal mouse would not do. This suggested the animal was still able to feel the initial pain stimulus but separated from an emotional response as it didn't permanently withdraw from the source of stimulus.
All of this implies that, while the animals could still effectively feel, and respond to, external pain stimuli, they were not emotionally bothered by it. It is still yet to be established whether this same neurological mechanism is found in humans, but the next stage for the researchers is to answer that very question. And if verified, it will open entirely new pathways for future pain research and treatment. Being able to silence the emotional sensation of pain while retaining the physical sensation would revolutionize treatments for chronic pain sufferers.
"Our big future hope is that the cells in the basolateral ensemble could be a tactic to curb the ailment of pain without causing addiction and thus, ideally, act as a possible substitute for opioid treatment," says Scherrer.
The new research was published in the journal Science.
Source: Stanford Medicine
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