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Kappa Opioid Receptor‐Based Treatments for Pain (LB88)
Author(s) -
Assana C.,
Feller C.,
Fogel M.,
Frelka A.,
Gottfried S.,
Jaber R.,
Keyes M.,
Koehler M.,
Kujawa K.,
Lautz N.,
Olson S.,
Pena J.,
Ries L.,
Schauer L.,
Scherrer C.,
Strandberg C.,
Strandberg S.,
Cunningham Christopher
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb88
Subject(s) - κ opioid receptor , hallucinogen , addiction , signal transduction , receptor , opioid , μ opioid receptor , opioid receptor , pharmacology , neuroscience , medicine , chemistry , psychology , biochemistry
Dangerous painkillers may cause serious problems for those who fall into drugs’ addictive trap, such as former NFL quarterback Brett Favre. The addictiveness of painkillers such as OxyContin and Vicodin is largely attributed to the response they trigger in proteins such as mu opioid receptors (MOPs). This receptor activates cellular signaling pathways responsible for dulling pain; however, the protein also has the ability to stimulate cellular signaling pathways that makes MOP‐based painkillers rewarding. An alternate target that alleviates pain but does not produce reward is the kappa opioid receptor (KOP). Unfortunately, many KOP agonists also activate signaling pathways that produce hallucinogenic effects. To investigate the changes that occur when KOP binds to different ligands, the Divine Savior Holy Angels SMART (Students Modeling A Research Topic) Team has used 3D printing technology to model the active site of the KOP with salvinorin A, to see how the induced fit changes the signal transduction pathways in a neuron. Manipulating receptor proteins like the KOP to inhibit pain pathways without the addictive effect of MOP‐targeting painkillers would be a breakthrough in chronic pain management. Computer‐aided drug design helps streamline the development of KOP ligands that activate this receptor in ways that result in less hallucinogenic effects. Grant Funding Source : Supported by a grant from NIH‐CTSA.