Cognitive theories of depression (e.g., 1
) posit that negative cognitions, derived from dysfunctional self schemas, play a central role in the etiology and course of this disorder. These dysfunctional schemas are hypothesized to bias information processing in depression, with depressed individuals selectively attending to and remembering affectively negative material. Indeed, there is strong evidence that depressed individuals are characterized by negative biases in memory, demonstrating better memory for negative material than do nondepressed individuals, (e.g., 2
). Importantly, several theorists have proposed that selective memory for negative information in depression contributes to the duration and severity of depressive episodes, (e.g., 5
Despite these consistent findings, we know little about the neural underpinnings of enhanced memory for negatively valenced stimuli in depressed relative to nondepressed individuals. Both lesion and functional neuroimaging studies confirm that the amygdala plays an important role in bolstering memory for emotional material. Cahill and his colleagues (7
), for example, reported that the generally better recall of affectively valenced than of neutral information is sharply attenuated in patients with lesions confined to the amygdala. Furthermore, using fMRI, Canli found amygdala responsivity to predict subsequent memory performance for affective stimuli both across individuals (9
) and across trials (10
Several investigators have posited that the amygdala facilitates memory for emotional stimuli through modulation of the hippocampus, a structure crucial for episodic memory encoding, (e.g., 11
). Packard, Cahill, and McGaugh (12
), for example, showed that amygdala stimulation following training facilitated hippocampal-mediated learning in rats and was not blocked by anesthetizing the amygdala prior to a retention test, indicating that the resulting pro-mnemonic effects were not due to lasting changes within the amygdala itself. These findings of amygdala facilitation of hippocampal-dependent learning are echoed in neuroimaging studies of humans by investigators reporting a significant correlation between activation of the amygdala and hippocampus during successful encoding of affective stimuli (13
The amygdala has also been found to facilitate learning that is dependent on the putamen and caudate, (e.g., 12
), a structure complex centrally involved in skill learning, (e.g., 16
). Packard and Teather (15
), for example, found that amygdala stimulation following training in rats facilitates caudate-putamen mediated learning and, further, that these memory bolstering effects are blocked by anesthetizing the caudate-putamen following training, but not by pre-test amygdala anesthetization. Moreover, given that the amygdala and caudate-putamen comprise nodes of the affective division of the cortico-striatal-pallidal-thalamic (CSPT) loop (17
), a circuit involved in the maintenance of information in working memory, (e.g., 18
), investigators have posited that the amygdala-caudate-putamen system subserves emotionally-mediated working memory.
The formulation that over-active amygdala-caudate-putamen and/or amygdala-hippocampus systems underlie enhanced memory for negative information in depression is also consistent with findings that depressed individuals have been characterized by greater responsivity to negative stimuli in the amygdala (19
), hippocampus (19
) and caudate-putamen (19
) than are nondepressed persons. The relevance of amygdala reactivity to memory in depression has been shown by Roberson-Nay et al. (23
) who found that, unlike their nondepressed peers, depressed adolescents showed greater amygdala reactivity when viewing faces that they subsequently remembered versus faces that they subsequently forgot.
The present study was designed to test a model of enhanced memory for negative stimuli in depression in which the neural mechanisms that are involved in bolstering encoding of emotionally valenced material in general are recruited more during encoding of negative material by depressed individuals. More specifically, we test a model in which amygdala activity and consequent modulation of the hippocampus and/or the caudate-putamen is increased during successful encoding of negative stimuli in depression. Based on the literatures reviewed above, we hypothesize that depressed individuals will exhibit better memory for negative material than will nondepressed individuals, as well as greater amygdala activation during successful encoding of negative material. Finally, we predict that amygdala activation during successful encoding of negative stimuli will be more strongly correlated with activation in the hippocampus and caudate-putamen in depressed than in nondepressed participants.