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Evidence that depression is associated with a blunted approach system comes from several sources. One of them is an earlier literature using EEG to examine anterior cortical asymmetry and motivational processes. This technique has far poorer spatial resolution than do newer imaging techniques, and thus it is far less specific about what areas are activated. However, it has been used to make a case concerning partial localization of approach and avoidance systems in left and right hemispheric areas, respectively (e.g., Davidson, 1998).
Previously depressed (Henriques & Davidson, 1990) and clinically depressed persons (Henriques & Davidson, 1991) have been found to have lower activation in left anterior cortical areas than do nondepressed persons, with no difference in right anterior activation. The lower activation was in areas that previous research had related to approach sensitivities (e.g., Coan & Allen, 2003; Harmon-Jones & Allen, 1997; Sutton & Davidson, 1997). This general pattern regarding depression has been replicated a number of times (J. J. Allen, Iacono, Depue, & Arbisi, 1993; Gotlib, Ranganath, & Rosenfeld, 1998), though not all attempts have been successful (Reid, Duke, & Allen, 1998). These findings as a group suggest that depression relates to low engagement of areas pertaining to approach. One recent study has even linked early-onset depression to a deficit in left prefrontal responsiveness to a task that had been designed specifically to engage approach motivation (Shankman, Klein, Tenke, & Bruder, 2007).
Behavioral research also suggests that depression relates to blunted incentive sensitivity. For example, depressed persons were found to be less responsive to reward (though not to punishment) than were nondepressed persons (Henriques & Davidson, 2000; Henriques, Glowacki, & Davidson, 1994; see also Depue & Iacono, 1989). There is also evidence that dysphoric persons engage more effort at easy task levels than do nondysphoric persons, as though they overestimated the effort that is required by the task, but that dysphoric persons are more likely to disengage effort when the task actually is demanding (Brinkmann & Gendolla, 2008).
Other evidence relates self-reports of low incentive sensitivity to depression (Campbell-Sills, Liverant, & Brown, 2004; Pinto-Meza et al., 2006). Indeed, three separate studies have found that self-reports of low incentive sensitivity predicted worse course of depression over time (Campbell-Sills et al., 2004; Kasch, Rottenberg, Arnow, & Gotlib, 2002; McFarland, Shankman, Tenke, Bruder, & Klein, 2006).
Blunted approach motivation may also be reflected in low dopaminergic function. Dopaminergic pathways are believed to be critical in the engagement of goal-directed effort (Farrar et al., 2007; Salamone et al., 2007; Salamone, Correa, Mingote, & Weber, 2005; Salamone, Correa, Mingote, Weber, & Farrar, 2006). A weakly functioning dopaminergic incentive system yields less “wanting” for appetitive outcomes (Berridge, 2007) and less engagement of effort in pursuit of them (Salamone et al., 2005, 2006, 2007). A recent comprehensive review reported a range of evidence for deficits in the function of dopamine among depressed persons, drawing from pharmacological studies, genetic studies, and dopamine challenge studies (Dunlop & Nemeroff, 2007).
Animal research has long implicated subcortical reward pathways in behaviors that mimic depressive symptoms, such as diminished motivation, apathy, and poor appetite (Nestler & Carlezon, 2006). Some brain studies in humans also link depression to deficits in subcortical regions involved in reward sensitivity, such as the caudate. For example, in a recent fMRI study, children diagnosed with depression displayed less activation of the caudate throughout a task involving reward, compared with children without depression (Forbes, Fox, Cohn, Galles, & Kovacs, 2006). Adults with depression have been found to show hyperreactivity of the caudate and the putamen to an amphetamine challenge that was designed to intensify dopaminergic activity (Tremblay et al., 2005); this pattern is consistent with there being a baseline deficit in dopaminergic activity.
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