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Science. 2019 Jan 18;363(6424):276-281. doi: 10.1126/science.aap8586.

An amygdalar neural ensemble that encodes the unpleasantness of pain.

Corder G1,2,3,4, Ahanonu B5,6,7, Grewe BF5,7, Wang D1, Schnitzer MJ8,6,7,9, Scherrer G10,2,3,4,11.

Author information

1
Department of Anesthesiology, Perioperative, and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
2
Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA.
3
Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
4
Stanford Neurosciences Institute, Stanford University, Stanford, CA 94305, USA.
5
Department of Biology, Stanford University, Stanford, CA 94305, USA.
6
Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.
7
CNC Program, Stanford University, Stanford, CA 94305, USA.
8
Department of Biology, Stanford University, Stanford, CA 94305, USA. mschnitz@stanford.edu gs25@stanford.edu.
9
Department of Applied Physics, Stanford University, Stanford, CA 94305, USA.
10
Department of Anesthesiology, Perioperative, and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. mschnitz@stanford.edu gs25@stanford.edu.
11
New York Stem Cell Foundation-Robertson Investigator, Stanford University, Stanford, CA 94305, USA.

Abstract

Pain is an unpleasant experience. How the brain's affective neural circuits attribute this aversive quality to nociceptive information remains unknown. By means of time-lapse in vivo calcium imaging and neural activity manipulation in freely behaving mice encountering noxious stimuli, we identified a distinct neural ensemble in the basolateral amygdala that encodes the negative affective valence of pain. Silencing this nociceptive ensemble alleviated pain affective-motivational behaviors without altering the detection of noxious stimuli, withdrawal reflexes, anxiety, or reward. Following peripheral nerve injury, innocuous stimuli activated this nociceptive ensemble to drive dysfunctional perceptual changes associated with neuropathic pain, including pain aversion to light touch (allodynia). These results identify the amygdalar representations of noxious stimuli that are functionally required for the negative affective qualities of acute and chronic pain perception.

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