| First Author | Hnasko TS | Year | 2005 |
| Journal | Nature | Volume | 438 |
| Issue | 7069 | Pages | 854-7 |
| PubMed ID | 16341013 | Mgi Jnum | J:103809 |
| Mgi Id | MGI:3610756 | Doi | 10.1038/nature04172 |
| Citation | Hnasko TS, et al. (2005) Morphine reward in dopamine-deficient mice. Nature 438(7069):854-7 |
| abstractText | Dopamine has been widely implicated as a mediator of many of the behavioural responses to drugs of abuse. To test the hypothesis that dopamine is an essential mediator of various opiate-induced responses, we administered morphine to mice unable to synthesize dopamine. We found that dopamine-deficient mice are unable to mount a normal locomotor response to morphine, but a small dopamine-independent increase in locomotion remains. Dopamine-deficient mice have a rightward shift in the dose-response curve to morphine on the tail-flick test (a pain sensitivity assay), suggesting either a decreased sensitivity to the analgesic effects of morphine and/or basal hyperalgesia. In contrast, dopamine-deficient mice display a robust conditioned place preference for morphine when given either caffeine or l-dihydroxyphenylalanine (a dopamine precursor that restores dopamine throughout the brain) during the testing phases. Together, these data demonstrate that dopamine is a crucial component of morphine-induced locomotion, dopamine may contribute to morphine analgesia, but that dopamine is not required for morphine-induced reward as measured by conditioned place preference. |
