Attention-Deficit Hyperactivity Disorder (ADHD) is the most common childhood psychiatric disorder, and one that, left untreated, is associated with low socio-economic status, addiction and/or incarceration. Our lab has created a construct valid mouse model based on the Slc6a3tm1Rbl (DAT Val559) coding variant to elucidate neurobiological mechanisms supporting ADHD and other DA-linked comorbid disorders. With these 129;B6-Slc6a3tm1Rbl animals and their wildtype adolescent littermates, we sought evidence for cognitive, attention and impulsivity alterations using the 5 choice serial reaction time task (5-CSRTT) and used progressive ratio and sucrose preference tasks to examine changes in motivation and hedonic valuation. In the 5-CSRTT, mice were trained to a baseline performance with a 5 second delay followed by a 2 second stimulus presentation. Premature, incorrect, and correct responses were recorded, as well as, omissions. Once animals met predetermined criteria for task completion, the paradigm was manipulated to probe for different aspects of attention and impulsivity. This effort consisted of increasing the delay between the start of the trial to the presentation of the stimulus from 5 seconds to 15 seconds. Mice were also tested under a variable delay condition where four different delay times (2, 5, 10, and 15 seconds) were used throughout the session in a randomized order. DAT Val559 mice showed several key differences in the task, including faster acquisition of the task, increased impulsivity under the long delay condition, yet improved performance with a variable delay. We hypothesize that with the proper motivation, DAT Val559 may hyperfocus on the parameters driving task acquisition and differentially utilize the temporal information presented during training sessions, being less reliant on absolute timing expectations. An enhancement in motivation for reward in the DAT Val559 mice was suggested by an increase in the progressive ratio break point. Interestingly this response became dysregulated under a devalued condition (i.e. DAT Val559 mice will continue to nose-poke for reward despite home cage satiation). This alteration is likely not due to a difference in hedonic valuation as we found no genotype difference in sucrose preference. Ongoing studies seek to determine the cellular and circuit level plasticities that derive from lifelong expression of the DAT Val559 variant and that lead to the observed changes in impulsivity and motivation. Supported by NIH Awards MH107132-02 (GLD) MH105094 (RDB).