1. Graduate Program in Neurobiology & Behavior,
2. Howard Hughes Medical Institute, and
3. Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA

Correspondence to: Richard D. Palmiter^2,3 Correspondence and requests for materials should be addressed to R.D.P. (Email: palmiter@u.washington.edu).

Dopamine has been widely implicated as a mediator of many of the behavioural responses to drugs of abuse¹. 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.

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