About DD mice

The dopamine deficient mouse model was developed in the lab of Dr. Richard Palmiter at the University of Washington.

Frequently asked questions about DD mice

  • Q: Are DD mice “knockouts”?
  • Q: How and why are DD mice treated with L-dopa?
  • Q: Is there dopamine in the brain of a DD mouse?
  • Q: If DD mice can’t move or eat, how can their behavior and feeding be studied?
  • Q: How can I obtain DD mice for study? A: Contact Dr. Cannon:

    • More information

  • Selected Publications
  • The genetics of dopamine-deficient mice, explained
  • Movies of mouse behavior
  • Preliminary Data


    • A dopamine deficient mouse from our colony

    More about dopamine, reward, and choice:
    The neurotransmitter dopamine has been identified as a primary mediator of brain reward circuits. In addition, dopamine has important effects on a wide range of motivated behaviors, including feeding, and has been implicated in the pathophysiology of human obesity. It has been suggested that dopamine is critical to learning about rewards, and that dopamine may mediate the “wanting”, or incentive motivational properties, of rewards.

    The DD mouse model offers a unique vantage from which we can study these processes. The reward-related behaviors of DD mice, e.g. sucrose preference, conditioned taste preference, and conditioned place preference, suggest that dopamine may not always be required for learning about or wanting rewards. It seems likely that DA plays an important role in the reward processes of intact animals. It also seems likely that non-dopaminergic mediators are sufficient for some reward processes.

    Dopamine-deficient mice demonstrate Parkinsonian behavioral deficits. These deficits may contribute significantly to the inability of DD mice to demonstrate normal levels of “wanting” for rewards. In other words, DD mice appear motivated to obtain rewards, and demonstrate normal reward-directed behaviors – when they do behave. DA acting within a nucleus of the basal ganglia called the subthalamic nucleus is critical for the brain’s ability to coordinate behavior. Normal signaling of neurons within the subthalamic area is critical for the ability to act on motivation. The subthalamic area appears to be important to response selection, and we are interested in whether alterations in neuronal signaling of the subthalamic nucleus may contribute to the pathophysiology of addictive behaviors.

    Questions or comments are welcomed. You may also contact Dr. Cannon at: