New research shows how the brain’s marijuana-like chemicals suppress pain

Part of the brain, usually associated with memory, plays an active role in suppressing pain during times of stress, according to research carried out at NUI Galway.

The new findings about how the brain functions to suppress pain were published in the leading journal Pain. The work was carried out by the researchers in pharmacology and therapeutics and the Centre for Pain Research at the National Centre for Biomedical Engineering Science at the university.

“In times of immense stress or fear, pain transmission and perception can be suppressed potently in humans and other animals,” explains a spokesperson for NUI Galway. “This important survival response can help us cope with, or escape from, potentially life-threatening situations. An increased understanding of the biological mechanisms involved in this so-called fear-induced analgesia is important from a fundamental physiological perspective and may also advance the search for new therapeutic approaches to the treatment of pain.”

Dr David Finn, co-director of the centre for pain research at NUI Galway, and study leader, says the body can suppress pain when under extreme stress, in part through the action of marijuana-like substances produced in the brain.

“What we have now identified for the first time is that the brain’s hippocampus is an important site of action of these endocannabinoids during the potent suppression of pain by fear. This research, which was funded by a grant from Science Foundation Ireland, advances our fundamental understanding of the neurobiology of pain and may facilitate the identification of new therapeutic targets for the treatment of pain and anxiety disorders.”

Working with Dr Finn, first author Dr Gemma Ford demonstrated that inhibition of the enzyme that breaks down one of these endogenous marijuana-like substances in the hippocampus had the effect of enhancing stress-induced pain suppression.

Further experimentation revealed that these effects were mediated by the cannabinoid CB1 receptor and were likely to be mediated by stress-induced increases in levels of endocannabinoids in the hippocampus.

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