Neurochemical Sample Clauses

Neurochemical. The role of neurochemicals in nocebo responses has been best shown in the field of pain. A series of studies have highlighted the role of the neurotransmitter cholecystokinin (CCK) in nocebo hyperalgesia responses (Xxxxxxxxx, Xxxxxxx, Xxxxxxxx, & Xxxxxxxxxx, 2006). In the first of these studies, postoperative patients were given proglumide, a CCK antagonist, during nocebo hyperalgesia induced by administration of saline solution which they were told would produce a pain increase (Xxxxxxxxx, Xxxxxxx, Xxxxxxx, Xxxxxx, & Xxxxx, 1997). This study found that the administration of proglumide prevented nocebo hyperalgesia in a dose-dependent manner, therefore suggesting that nocebo hyperalgesia is mediated by the transmission of CCK (Xxxxxxxxx et al., 1997). As CCK is involved in anxiety mechanisms it was thought that proglumide could also affect nocebo hyperalgesia by preventing the generation of anxiety about the impending pain (Xxxxxxxxx et al., 1997). To test this, Xxxxxxxxx et al. (2006) studied experimental ischemic arm pain in healthy volunteers and found that administration of an inert substance, along with verbal suggestions of hyperalgesia, induced hyperalgesia and activity of the hypothalamic-pituitary-adrenal (HPA) axis which is involved in the stress response. After administration of diazepam (an anti-anxiety drug), both HPA activity and nocebo hyperalgesia were blocked. However when just the CCK antagonist, proglumide, was given only hyperalgesia was prevented, there was no effect on the HPA axis (Xxxxxxxxx et al., 2006). This suggests that CCK does not act on nocebo-induced anxiety but, rather, on the nocebo/anxiety- induced hyperalgesia. Therefore proglumide does not block anticipatory anxiety of impending pain as previously thought, and instead must interrupt the link between anxiety and pain (Colloca & Xxxxxxxxx, 2007). As well as CCK, endogenous opioids and dopamine activity have been implicated in nocebo research. Xxxxxxxxx, Xxxxxxx, Xxxxxxx, and Colloca (2007) have found that verbal suggestions of a decrease in pain activates endogenous opioid neurotransmission, while suggestions of an increase in pain activates the CCK receptors. Supporting this, Xxxxx et al. (2008) has shown that placebo responses to a pain challenge are associated with greater dopamine activation (DA) and opioid activity, whereas nocebo responses are associated with deactivations of dopamine and a decrease in opioid release.
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