Stress-Induced Analgesia

Abstract

Abbreviations: SIA, stress-induced analgesia; FCA, fear-conditioned analgesia; GABA, Ȗ-aminobutyric acid; HA, high analgesia; LA, low analgesia; fMRI, functional magnetic resonance imaging; DNIC, diffuse noxious inhibitory control; PAG, periaqueductal grey; RVM, rostroventral medulla; 5-HT, 5-hydroxytryptamine; CB 1 , cannabinoid type 1; CB 2 , cannabinoid type 2; NMDA, N-methyl-D-aspartic acid; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; mGluR, metabotropic glutamate receptor; NK1, neurokinin 1; SP, substance P; 2-AG, 2-arachidonoylglycerol; FAAH, fatty acid amide hydrolase; MGL, monoacylglycerol lipase; HPA, hypothalamo-pituitary-adrenal; ACTH, adrenocorticotropic hormone 3 ABSTRACT For over 30 years, scientists have been investigating the phenomenon of pain suppression upon exposure to unconditioned or conditioned stressful stimuli, commonly known as stress-induced analgesia. These studies have revealed that individual sensitivity to stressinduced analgesia can vary greatly and that this sensitivity is coupled to many different phenotypes including the degree of opioid sensitivity and startle response. Furthermore, stress-induced analgesia sensitivity can vary a great deal depending on age, gender, and prior experience to stressful, painful, or other environmental stimuli. Stress-induced analgesia is mediated by activation of the descending inhibitory pain pathway.Pharmacological and neurochemical studies have demonstrated involvement of a large number of neurotransmitters and neuropeptides. In particular, there are key roles for the HQGRJHQRXV RSLRLG PRQRDPLQH FDQQDELQRLG Ȗ-aminobutyric acid and glutamate systems. The study of stress-induced analgesia has enhanced our understanding of the fundamental physiology of pain and stress and has been a useful approach for uncovering new therapeutic targets for the treatment of pain and stress-related disorders.4