By F Benedetti; Christoph Stein; et al
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Extra resources for Analgesia
A suggested mechanism includes the activation of PLC, generating diacylglycerol that binds to PKCε, leading to its phosphorylation. PKCε can then signal to matrix metalloproteinases, which can cleave Opioids 39 membrane-anchored epidermal growth factor receptor (EGF)-type ligands, thereby initiating EGF receptor transactivation and ultimately activation of the MAPK phosphorylation cascade (Belcheva et al. 2005; Pierce et al. 2001). So far, little is known about the functional signiﬁcance of this phenomenon.
9 Side Effects . . . . Acute Opioid Application Cardiovascular System . Respiratory System . . Sedation . . . . . Nausea and Vomiting . Cough Suppression . . Pupil Constriction . . Skeletal Muscle Rigidity .
In 1942 the substitution of an allyl group for the methyl group on the nitrogen atom of morphine produced the ﬁrst opioid receptor antagonist, nalorphine. Nalorphine not only countered the effects of morphine but also produced limited analgesia mediated through κ-opioid receptors. An additional member of this mixed agonist/antagonist group is buprenorphine, a semi-synthetic opiate derivative of thebaine. Buprenorphine is a partial agonist at the μ-receptor. At low doses it produces typical morphine-like effects, and at higher doses it has a reduced intrinsic activity compared to pure agonists (Cowan et al.
Analgesia by F Benedetti; Christoph Stein; et al