Central Amygdala CeAGA Neurons: A Critical Circuit for Pain Suppression and Potential Targets for Novel Analgesic Therapies

A study on mice showed that the activation of neurons called CeAGA makes it possible to suppress pain in rodents.

“Many people think there’s a central area that relieves pain,” says neurobiologist Fan Wang, “which is why placebos work.” The scientific community has been searching for the location of this area, and Professor Wang’s team may have found the answer. According to research published in Nature Neuroscience, it could be the amygdala, an area of the brain associated with emotions like fear and anxiety.

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The Role of CeAGA

“Most previous studies have focused on areas activated by pain,” says Wang. However, many areas are responsible for pain, and all need to be inactivated to stop it—except this area, which can eliminate pain by itself. To understand the role of the amygdala, Fan Wang and his team analyzed the effects of general anesthesia on neurons. They found that it activates a subset of inhibitory neurons in the amygdala, known as CeAGA neurons. These neurons are linked to several other areas of the brain. By artificially stimulating pain in rats, they were able to map the areas connected to CeAGA neurons.

Immediate Effects

“Pain is a complex brain reaction,” says Wang, “involving sensory, emotional, and automatic responses of the nervous system.” Optogenetics, a technique that uses light to act on nerve cells, enabled the team to bypass these brain reactions in rats. For example, by activating CeAGA neurons, the rats immediately stopped licking their paws or grooming their heads. “It’s radical,” stresses Wang, “they stopped immediately!”

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A New Class of Painkillers

The researchers also discovered that these neurons are crucial for the effect of painkillers. For instance, low-dose ketamine, used as an analgesic, stimulates them. However, the effectiveness of ketamine is nullified when these neurons are inactivated. Wang’s team now aims to continue their research to develop a treatment that specifically activates CeAGA neurons. This could lead to a new class of painkillers.