Summary: Researchers find brain areas associated with pain and empathy may be involved in the social transfer of pain in mice.
Pain sensitivity associated with alcohol withdrawal may activate the same brain region in both drinking and non-drinking mice, finds a study published in eNeuro.
Monique Smith and colleagues previously showed that “bystander” mice housed with mice undergoing withdrawal from opioids or alcohol experience hyperalgesia, a heightened sensitivity to pain, just like the induced-withdrawal mice. In this study, the authors explored whether brain regions associated with pain and empathy for pain in humans — the somatosensory cortex, insula (INS), and anterior cingulate cortex (ACC) — might be involved in the social transfer of pain in mice.
Smith and colleagues compared the brain activity of “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 ACC and INS. The authors found that inhibiting activity in the ACC reversed hyperalgesia in both primary and bystander mice. These results suggest a potential neural overlap between physically-induced and socially-transferred hyperalgesia.
Source: David Barnstone – SfN
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Original Research: Abstract for “Anterior Cingulate Cortex Contributes to Alcohol Withdrawal-Induced and Socially Transferred Hyperalgesia” by Monique L. Smith, Andre. T. Walcott, Mary M. Heinricher and Andrey E. Ryabinin in eNeuron. Published online July 24 2017 doi:10.1523/ENEURO.0087-17.2017
Anterior Cingulate Cortex Contributes to Alcohol Withdrawal-Induced and Socially Transferred Hyperalgesia
Pain is often described as a “biopsychosocial” process, yet social influences on pain and underlying neural mechanisms are only now receiving significant experimental attention. Expression of pain by one individual can be commun-icated to nearby individuals by auditory, visual, and olfactory cues. Conversely, the perception of another’s pain can lead to physiological and behavioral changes in the observer, which can include induction of hyperalgesia in “bystanders” exposed to “primary” conspecifics in which hyperalgesia has been induced directly. The current studies were designed to investigate the neural mechanisms responsible for the social transfer of hyperalgesia in bystander mice housed and tested with primary mice in which hyperalgesia was induced using withdrawal from voluntary alcohol consumption. Male C57BL/6J mice undergoing withdrawal from a 2-bottle choice voluntary alcohol-drinking procedure served as the primary mice. Mice housed in the same room served as bystanders. Naïve, water-drinking controls were housed in a separate room. Immunohistochemical mapping identified significantly enhanced Fos immunoreactivity in the anterior cingulate (ACC) and insula (INS) of bystander mice compared to naïve controls, and in the dorsal medial hypothalamus (DMH) of primary mice. Chemogenetic inactivation of the ACC but not primary somatosensory cortex reversed the expression of hyperalgesia in both primary and bystander mice. These studies point to an overlapping neural substrate for expression of socially transferred hyperalgesia and that expressed during alcohol withdrawal.
Significance Statement Pain is not a direct function of tissue damage, and is highly influenced by psychosocial context. Social influences on pain and underlying neural mechanisms have received limited attention in animal studies, although the available data suggest that social influences on pain in rodents are complex and bidirectional, as in humans. The present studies investigated mechanisms underlying hyperalgesia associated with alcohol withdrawal, and with socially transferred hyperalgesia in bystander animals housed and tested in the same room, both of which could be considered “top-down” drivers of enhanced pain responding. Neural activity was differentially enhanced in the two groups, but chemogenetic inactivation pointed to an at least partially overlapping substrate for withdrawal-related and socially transferred hyperalgesia in the anterior cingulate cortex.
“Anterior Cingulate Cortex Contributes to Alcohol Withdrawal-Induced and Socially Transferred Hyperalgesia” by Monique L. Smith, Andre. T. Walcott, Mary M. Heinricher and Andrey E. Ryabinin in eNeuron. Published online July 24 2017 doi:10.1523/ENEURO.0087-17.2017