Bipolar spectrum disorders (BSDs) are defined by extreme and opposing states of mood, motivation, behaviour and cognition occurring within the same individual (Alloy & Nusslock, 2019). BSDs are chronic and severe psychiatric disorders; the majority of adults with BSDs experience high levels of functional impairment and levels of comorbidity are approximately three times higher than the general population (Gitline and Miklowitz, 2017; Martino et al., 2017). BSD symptoms have been shown to occur on a spectrum that extends from the general population to milder forms of BSD (cyclothymic disorder) to more severe forms (bipolar I disorder) (Akiskal et al., 2000; Angst & Gamma, 2002). Given the prevalence and significant impairment associated with BSDs, there is a substantial need for further research to better understand the mechanisms underlying BSDs. One of the most well-established theories of BSDs is the reward hypersensitivity model, which argues that BSDs are characterised by increased reactivity to goal- and reward-relevant cues (e.g. Alloy, Olino, Freed & Nusslock, 2016; Depue & Iacono, 1989; Depue, Krauss, & Spoont, 1987; Johnson, 2005; Johnson, Edge, Holmes, & Carver, 2012). This model can account for both manic and depressive episodes in BSD; reward-activation stimuli (internal or external) can result in excessive approach-related affect, behaviour and motivation, and ultimately result in hypo/manic symptoms e.g. decreased need for sleep or increased energy. Conversely, reward-deactivation events can lead to excessive down-regulation of approach-related affect, behaviour and motivation which can result in depressive symptoms e.g. anhedonia and hopelessness. Thus, a hypersensitivity to internal or external cues signalling potential gain or loss of reward, and a tendency towards excessive activation and deactivation of the reward system confer a vulnerability to the development of BSDs (Alloy & Nusslock, 2019). Several lines of evidence support the reward hypersensitivity model. Briefly, individuals with or at high risk for BSDs report greater self-reported, behavioural, emotional, cognitive, and neurophysiological responses to rewards vs. healthy controls. (see Nusslock & Alloy, 2017 for a recent review). For example, increased reward sensitivity has been shown to predict onset of BSDs (Alloy et al., 2012a) and is associated with clinical severity and impairment in BSDs (Alloy et al., 2012b). Further, in individuals with BSDs, reward-activating events have been found to predict hypo/manic symptoms or episode onset, however positive events in general did not, and reward-deactivating events were found to precipitate depressive episodes (Alloy et al., 2015; 2016). Recent neuroimaging research has provided mixed support for the reward hypersensitivity model of BSDs (see Nusslock & Alloy, 2017 for review). For example, functional MRI (fMRI) studies using reward-based paradigms have reported elevated activation in the ventral striatum and the orbitofrontal cortex, which are implicated in encoding and anticipating rewards and assessing the value and probability of reward outcomes respectively (Diekhof, Kaps, Falkai, & Gruber, 2012), in individuals with BSDs (see Alloy et al., 2016; Nusslock & Alloy, 2017 for reviews). Therefore, there appears to be some evidence supporting a relationship between BSDs and elevated activation in the fronto-striatal reward circuit, however, it is important to note that despite replication of increased prefrontal activation to reward, there are inconsistent findings for striatal activation; some studies have reported increased activation (Nusslock et al., 2012; Singh et al., 2013; Dutra, Cunningham, Kober & Gruber, 2015), some have reported decreased activation (Abler et al., 2008; Johnson, Mehta, Ketter, Gotlib & Knutzon, 2019), and still others have reported no difference between BSDs and healthy controls (Bermpohl et al., 2010). Studies using at-risk populations have reported similarly inconsistent findings. For example, Singh et al. (2014), reported decreased activation in and connectivity between reward-related regions during anticipation of loss and greater activation in orbitalfrontal cortex during reward receipt, whereas Soehner et al. (2016), found elevated connectivity during reward receipt. A number of factors may help to explain these discrepant findings. Firstly, studies of clinical populations of BSDs typically categorise participants as being in euthymic, manic or depressive episodes. However, although symptoms levels may not reach threshold for manic or depressive episodes, participants may be experiencing both symptoms. Thus, hypo/manic and depressive symptoms may have an impact on reward processing, however, previous studies have not had sufficient power to tease apart this relationship (Alloy & Nusslock, 2019). Secondly, clinical populations of BSDs are typically in receipt of antidopaminergic medications. As dopamine is a key neurotransmitter in the reward system, medications which regulate its transmission may result in neural adaptations within the reward system, which may explain discrepant findings (Mason, O’Sullivan, Bentall & El-Deredy, 2012). Additionally, differences in methodology may limit the comparability of results; for example, some studies utilized a card-guessing fMRI paradigm, which includes a decision-making component, whereas others utilized the monetary incentive delay fMRI, where only a button press to a target is required. Thus, regions within the neural reward circuitry may be differentially activated depending on the paradigm utilized in a given study and the different processes they recruit. The current study seeks to address each of the above issues by examining the relationship between reward processing and hypo/manic and depressive symptoms longitudinally in a large (N > 1500) community-based sample, using a monetary incentive delay (MID) fMRI paradigm. This study will examine subthreshold hypo/manic and depressive symptoms, and further, will examine their relationship with reward processing simultaneously, rather than classifying participants as being in distinct and disparate episodes. Moreover, this study will utilize a preclinical population to minimize the impact of antidopaminergic medication and will further control for this in analyses.