Journal
ENEURO
Volume 4, Issue 4, Pages -Publisher
SOC NEUROSCIENCE
DOI: 10.1523/ENEURO.0087-17.2017
Keywords
alcohol; anterior cingulate; empathy; pain; social; withdrawal
Categories
Funding
- NIAAA NIH HHS [P60 AA010760, P50 AA010760, R21 AA025548, R01 AA019793, F31 AA022824, T32 AA007468, R01 AA025024] Funding Source: Medline
- NINDS NIH HHS [R01 NS066159, R56 NS093894] Funding Source: Medline
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Pain is often described as a biopsychosocialprocess, yet social influences on pain and underlying neural mechanisms are only now receiving significant experimental attention. Expression of pain by one individual can be communicated 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 bystandersexposed to primaryconspecifics 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 (WD) from voluntary alcohol consumption. Male C57BL/6J mice undergoing WD from a two-bottle choice voluntary alcohol-drinking procedure served as the primary mice. Mice housed in the same room served as bystanders. Naive, water-drinking controls were housed in a separate room. Immunohistochemical mapping identified significantly enhanced Fos immunoreactivity (Fos-ir) in the anterior cingulate cortex (ACC) and insula (INS) of bystander mice compared to naive 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 WD.
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