Pain is an unpleasant sensory and emotional experience caused by stimulating nerve receptors contained within tissue damaged by trauma. Usually pain dissipates once the traumatic stimulus is removed and the body has healed, however, pain can persist after the wound has healed, and has been shown to arise even without pathology. Pain-based response in the brain involves multiple regions and connections making the treatment of pain particularly difficult and impersonal in some cases, with the silencing of all of these brain regions simultaneously proving challenging. Therefore, much work is currently being performed to find a center in the brain possessing the ability to switch off multiple regions involved in processing pain at the same time. Now, a study from researchers at Duke University identifies a pain-suppression center in the brain possessing widespread projections to many pain-processing centers throughout the central nervous system. The team states this newly discovered brain center switches pain off and is located in the amygdala, often considered the home of negative emotions and responses, such as the fight or flight response and general anxiety. The study is published in the journal Nature Neuroscience.
Recent studies from the group found general anesthesia promotes slow-wave sleep by activating the supraoptic nucleus of the brain. However, sleep and pain are thought to be separate, with these atypical results leading to the finding pain can be repressed by general anesthesia (GA) without inducing loss of consciousness. Therefore, the group investigated supraspinal analgesic circuits involved in the modulation and production of analgesia of the body consisting of many brain regions, including the amygdala. The amygdala also plays important roles in emotional responses, stress, and anxiety believed to be a critical component in the manifestation of pain. The current study shows GA activates a specific subset of pain inhibitory neurons in the central amygdala, dubbed CeAga neurons.
The current study determines the presence of pain suppressing neurons in mice activated by GA in the amygdala using in vivo calcium imaging. The paths of activated CeAga neurons in the mice were then tracked to map connections to different parts of the brain. This was achieved by giving mice a mild noxious stimulus, activating brain regions responsible for processing pain. Results map at least sixteen brain centers known to process the sensory or emotional aspects of pain receiving inhibitory input from the CeAga neuronal circuit.
Data findings show when the activity of these CeAga neurons is inhibited the mice respond as if a minor trauma has become intense or painful. The lab states they also observed low-dose ketamine, an anesthetic known to allow sensation whilst blocking pain, activated the CeAga pain center; with this pharmaceutical losing its potency when these neurons were switched off.
The team surmises they have pinpointed a single off switch capable of quelling the response of dozens of pain-promoting areas contained within the brain, in effect making this switch a pain center. For the future, the researchers state they now plan to prospect for therapeutics capable of activating only these cells to subdue pain regions throughout the central nervous system.
Source: Duke University
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