The “switch” acts more like a “pain rheostat,” similar to a home thermostat that modulates temperature — the pain rheostat reacts to pain signals to modulate pain sensations. In the mice, researchers found that activity in neurons that express protein kinase C-delta (CeA-PKCδ) turned up the pain rheostat and demonstrated an increase in pain-related responses. Conversely, researchers found that activity in neurons that express somatostatin (CeA-Som) turned down the pain rheostat, inhibiting nociception or the chain of activity in the nerves required to communicate pain.

During the experiments, researchers were able to take advantage of molecular genetic approaches that allow them to fluorescently label and manipulate the activity of these two central amygdala cell types. They found that when they blocked CeA-PKCδ neurons, pain activity decreased. When researchers activated CeA-Som neurons, they observed a marked analgesic response in mice.

Do these findings have any immediate practical benefit for humans?