A new study finds a potential neural overlap between physically induced and socially transferred increased sensitivity to pain, or hyperalgesia. Previous research has shown that pain sensitivity associated with alcohol withdrawal can be communicated to nearby individuals by olfactory cues. But how this social transfer of pain occurs is not known.
Scientists at OHSU have now demonstrated that pain and empathy for pain activate partially overlapping regions of the brain in mice. Andrey Ryabinin, Ph.D., a professor of behavioral neuroscience in the OHSU School of Medicine, and Ph.D. candidate Monique Smith report in the journal eNeuro that those experiences are reversed by inhibiting activity in one region of the brain—the anterior cingulate cortex.
The researchers first mapped changing activity in brain regions associated with pain and empathy for pain and then inhibited some of the activated brain regions. Brain activity of three groups of mice were monitored: primary mice with access to increasing concentrations of ethanol, bystander mice housed in the same room, and control mice housed in a separate room. The primary mice showed increased activity in the dorsal medial hypothalamus when access to alcohol was removed, which may indicate a role for this area in alcohol withdrawal. In contrast, bystander mice showed increased activity in the anterior cingulate cortex and insula. Inhibiting activity in the anterior cingulate cortex reversed hyperalgesia in both primary and bystander mice.
One important observation: The two forms of hyperalgesia in this study do not have a basis in tissue or nerve injury. Rather, the results confirm that withdrawal-related hyperalgesia can be socially transferred in mice housed together. These findings set the stage for research to determine if there are distinct circuits within the anterior cingulate cortex that govern physically induced and socially transferred hyperalgesia.
This work was supported by the National Institutes of Health 1F31AA022824 (to M.L.S), AA019793, AA025548, and 6P60 AA10760 (to A.E.R.) and NS066159 and NS093894 (to M.M.H.).