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The pain is a complicated experience. Our skin and muscles feel it just as they feel softness or warmth. But unlike other sensations, the experience of pain is clearly unpleasant.
The pain must hurt so that we can pay attention and avoid further injury.
But for people with chronic pain, the pain has largely lost its raison d'être. It hurts.
Although it's been known for a long time how nerves signal pain in the brain, scientists do not know how the brain adds a layer of discomfort.
Results of a study published Thursday in Science offer an answer. A team of researchers at Stanford University identified the neurons in the brains of pain-injuring mice that could modify these neurons to reduce the discomfort of pain without eliminating sensation. The study lays the groundwork for future research on more targeted pain treatments.
"This study is a breakthrough," says Irene Tracey, neuroscientist of pain at Oxford University, who did not participate in the study. "It was a tour de force and a welcome addition to understand this complex and major problem."
Grégory Scherrer, neuroscientist at Stanford, who led the study, began researching pain neurons in the amygdala – the thin almond-shaped region that scientists know how to regulate many emotions. For Scherrer, the challenge was to sift through the entanglement of neurons and identify those badociated with the pain.
To do this, he teamed up with his Stanford colleague, Mark Schnitzer, a neuroscientist who has developed a miniature microscope, or miniscope, that can be attached to the head of a free-acting mouse.
"The miniscope allows you to track neurons over time, while the mouse behaves normally," says Schnitzer.
To see neuronal activity, the researchers first injected a fluorescent protein into the amygdala that releases a tiny discharge of light when the neurons are triggered. Then the team guides this thin, deep object into the brain to see what neurons are flashing when the mouse reacts to painful stimuli, such as needle sticks.
When a mouse is in pain, she retires reflexively, just as our hand does when we touch a hot stove. Scherrer says that these reflexive behaviors indicate the sensation of pain, but are not unpleasant. Other behaviors, such as avoiding the painful stimulus or licking the paw that touched it, indicate that the pain is unpleasant.
The researchers exposed the mice to a variety of mild and painful stimuli and identified a constellation of about 150 neurons in a region called the basolateral tonsil that were active only when the mice appeared to be suffering. In addition, it seemed that the more the mouse felt pain, the more this BLA constellation was glowing.
"At this point, we could only see that these BLA neurons correlated with pain," says Scherrer, "but not if they coded the inconvenience of pain."
To answer this question, the research team had to somehow turn off the pain neurons when the animal was suffering and see if the mouse was behaving differently.
Scherrer and his team have created chemical switches to control these painful neurons. They could then turn off those painful neurons and see if a mouse was behaving differently when it was pricking itself.
Getting these switches on the neurons of pain, and only the neurons of pain, required some genetic tricks. "This article really combines the most advanced techniques in neuroscience," says Jordan McCall, a neuroscientist at Washington University in St. Louis, who did not participate in the study.
With the switches in place, the researchers turned off the BLA pain neurons and found that the mice still felt the pain, but they did not behave as if they were uncomfortable.
"They did not care about pain anymore," says Scherrer.
This result resisted when the researchers examined mice that developed chronic pain. Their BLA pain neurons had become so sensitive that they were shooting at the slightest touch. When Scherrer deactivated their BLA neurons, the mice still felt the light touch, but did not seem to feel it unpleasant.
"This result really enthused us," says Scherrer, explaining that their findings suggest that the discomfort of acute and chronic pain comes from these BLA pain neurons, making it a target for treating pain.
Opioids can be effective in relieving pain, but they are a dull tool and affect areas of the brain badociated with behaviors as diverse as dependence and breathing, for example. "Now that we know that neurons give pain its annoyance, we can look for receptors found only in these neurons and not in other areas of the brain," says Scherrer.
If there are unique receptors for these neurons, researchers could try to design drugs that slow down their activity. If this approach works, it could lead to a drug that makes the pain more bearable, but does not cause a dull feeling, according to Schnitzer.
Treatment like this is far away, even under the best of circumstances. Although this research confirms that BLA neurons play a critical role in pain, they could work in concert with other areas of the brain that need to be understood. Scherrer and his colleagues are working on these links to get a more complete picture.
The research team is already looking for unique receptors for BLA pain neurons. "The question of whether we will find them is open," says Scherrer. "But I hope that out of 30,000 genes, there will be a couple coding for receptors that we can target for treatment."
Jonathan Lambert is an intern at NPR's Science Desk. You can follow him on Twitter: @evolambert.
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