Abstract
Morphine is widely used clinically for the treatment of severe pain. Bohn et al . show that this analgesic effect of morphine is enhanced in mice that lack the protein β-arrestin 2. Morphine produces its effects by binding to the μ opioid receptor, a heterotrimeric guanine nucleotide binding protein (G protein)-coupled receptor. However, the receptor has a desensitization mechanism through which it becomes phosphorylated and then interacts with the signaling inhibitor β-arrestin 2. There are actually four related arrestins, but animals lacking just β-arrestin 2 showed increased and prolonged pain-relieving effects of morphine. Thus, β-arrestin 2 appears to show specificity for the μ opioid receptor and to be required for its normal physiological response. Bohn, L.M., Lefkowitz, R.J., Gainetdinov, R.R., Peppel, K., Caron, M.G., and Lin, F-T. (1999) Enhanced morphine analgesia in mice lacking β-arrestin 2. Science 286 : 2495-2498. [Abstract] [Full Text]
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