The precise functional role of the hippocampus remains a topic of much debate. According to a dominant view, the dorsal/posterior hippocampus is implicated in memory and spatial navigation and the ventral/anterior hippocampus mediates anxietyrelated behaviours. However, this 'dichotomy view' may need revision. Gene expression studies demonstrate multiple functional domains along the hippocampal long axis, which often exhibit sharply demarcated borders. By contrast, anatomical studies and electrophysiological recordings in rodents suggest that the long-axis is organized along a gradient. Together, these observations suggest a model in which functional long-axis gradients are superimposed on discrete functional domains. This model provides a potential framework to explain and test the multiple functions ascribed to the hippocampus.The hippocampus is a medial temporal lobe structure critically involved in episodic memory and spatial navigation [1][2][3][4][5][6][7] . Its long, curved form is present across all mammalian orders and runs along a dorsal (septal) to ventral (temporal) axis in rodents, corresponding to a posteriorto-anterior axis in humans (FIG. 1a-b). The same basic intrinsic circuitry is maintained throughout the long axis and across species (FIG. 1c). Despite this conserved intrinsic circuitry, the dorsal and ventral portions have different connectivities with cortical and subcortical areas, and this has long posed a question as to whether the hippocampus is functionally uniform along this axis. Here we review cross-species data that show how the seemingly disparate functions ascribed to the hippocampus can be accommodated by a model in which different functional properties exist along the longitudinal axis.The severe memory impairment suffered by patient H.M. following bilateral hippocampal resection 1 led to intensive study 8 of patients and animal models with hippocampal damage, with an ensuing characterisation of hippocampal function in terms of declarative memory 2 , encompassing both episodic and semantic memory. At the same time, however, evidence emerged for a hippocampal role in spatial memory, based on the discovery of hippocampal 'place cells' 9,10 and the demonstration that hippocampal lesions impair spatial memory 4 . Both the declarative memory hypothesis 11 and the spatial mapping hypothesis 12 of hippocampal function proposed a unitary model in which the entire hippocampus is dedicated

Successful social interaction partly depends on appraisal of others from their facial appearance. A critical aspect of this appraisal relates to whether we consider others to be trustworthy. We determined the neural basis for such trustworthiness judgments using event-related functional magnetic resonance imaging. Subjects viewed faces and assessed either trustworthiness or age. In a parametric factorial design, trustworthiness ratings were correlated with BOLD signal change to reveal task-independent increased activity in bilateral amygdala and right insula in response to faces judged untrustworthy. Right superior temporal sulcus (STS) showed enhanced signal change during explicit trustworthiness judgments alone. The findings extend a proposed model of social cognition by highlighting a functional dissociation between automatic engagement of amygdala versus intentional engagement of STS in social judgment.

The influence of emotion on human memory is associated with two contradictory effects in the form of either emotion-induced enhancements or decrements in memory. In a series of experiments involving single word presentation, we show that enhanced memory for emotional words is strongly coupled to decrements in memory for items preceding the emotional stimulus, an effect that is more pronounced in women. These memory effects would appear to depend on a common neurobiological substrate, in that enhancements and decrements are reversed by propranolol, a ␤-adrenergic antagonist, and abolished by selective bilateral amygdala damage. Thus, our findings suggest that amygdaladependent ␤-adrenergic modulation of episodic encoding has costs as well as benefits. Substantial evidence indicates that enhanced memory for emotional experience engages a ␤-adrenergic system (1). ␤-Adrenergic blockade with the ␤ 1 ␤ 2 -antatgonist propranolol selectively impairs long-term human episodic memory for emotionally arousing material without affecting memory for a neutral story (2). This modulation of emotional memory by propranolol is centrally mediated, because peripheral ␤-adrenergic blockade has no such effect on emotional memory function (3). Human amygdala lesions also produce emotional memory impairment (4, 5), suggesting that this structure may represent a critical locus for propranolol's influence on emotional memory.Although emotionality is strongly associated with enhancements in memory, there is evidence for emotion-induced memory decrements (6,7). Human behavioral studies demonstrate enhanced memory for central details of an emotional event and memory suppression for peripheral details (8,9). Ecological studies show that details of an event are less likely to be remembered if followed by an emotional event (10). In experimental contexts a weak, although unreliable, effect on words presented in close proximity to potentially emotional items is reported (11). By contrast to the extensive literature on emotional enhancements in memory, nothing is known regarding the neurobiological processes accounting for emotion-induced impairments in memory.In a series of related experiments, we present psychological (Exp. 1), psychopharmacological (Exp. 2) and neuropsychological (Exp. 3) data that characterize the psychological and neurobiological properties of emotion-induced forgetting. Our first aim was to establish a behavioral index of emotion-evoked memory enhancement and impairment. In an initial behavioral memory experiment (Exp. 1), nouns were presented serially, every 3 s, in semantically related lists, and recall was tested after each list presentation. Each list, in this and subsequent experiments, contained two ''oddball'' nouns: an emotionally aversive noun (E noun) and a perceptual oddball noun (P noun), presented in a novel font (Fig. 1a). In line with previous observations (1, 6), memory for emotional items is enhanced relative to control nouns. Critically, items preceding E nouns (E-1 nouns) are recalled less well than cont...

We have studied patients with variable degrees of left hippocampal and amygdala pathology who performed a verbal encoding task during functional magnetic resonance imaging (fMRI) to assess the impact of pathology on emotional-memory performance and encoding-evoked activity. The severity of left hippocampal pathology predicted memory performance for neutral and emotional items alike, whereas the severity of amygdala pathology predicted memory performance for emotional items alone. Encoding-related hippocampal activity for successfully remembered emotional items correlated with the degree of left amygdala pathology. Conversely, amygdala-evoked activity with respect to subsequently remembered emotional items correlated with the degree of left hippocampal pathology. Our data indicate a reciprocal dependence between amygdala and hippocampus during the encoding of emotional memories.