The amygdala

Center for Neural Science, New York University, 4 Washington Place, New York, New York 10003, USA.
Current Biology (Impact Factor: 9.57). 11/2007; 17(20):R868-74. DOI: 10.1016/j.cub.2007.08.005
Source: PubMed
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    • "The CE serves as a major relay station to brainstem and hypothalamic regions that control threat responses engendered by the US alone (LeDoux, 2000; Maren, 2001; Davis and Whalen, 2001; Pare et al., 2004; Likhtik et al., 2008; Ehlich et al., 2009). Clusters of inhibitory GABAergic interneuronsdreferred to as the intercalated cell massesdalso mediate interactions between the LA and CE by gating fear expression (Millhouse, 1986; Sah et al., 2003; LeDoux, 2007; Ehlich et al., 2009). The amygdala contains reciprocal connections with surrounding brain regions to integrate sensory information and tailor conditioned fear responses appropriately across different circumstances. "
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    ABSTRACT: Fear learning and regulation is as a prominent model for describing the pathogenesis of anxiety disorders and stress-related psychopathology. Fear expression can be modulated using a number of regulatory strategies, including extinction, cognitive emotion regulation, avoidance strategies and reconsolidation. In this review, we examine research investigating the effects of acute stress and stress hormones on these regulatory techniques. We focus on what is known about the impact of stress on the ability to flexibly regulate fear responses that are acquired through Pavlovian fear conditioning. Our primary aim is to explore the impact of stress on fear regulation in humans. Given this, we focus on techniques where stress has been linked to alterations of fear regulation in humans (extinction and emotion regulation), and briefly discuss other techniques (avoidance and reconsolidation) where the impact of stress or stress hormones have been mainly explored in animal models. These investigations reveal that acute stress may impair the persistent inhibition of fear, presumably by altering prefrontal cortex function. Characterizing the effects of stress on fear regulation is critical for understanding the boundaries within which existing regulation strategies are viable in everyday life and can better inform treatment options for those who suffer from anxiety and stress-related psychopathology.
    01/2015; 1(1):134-146. DOI:10.1016/j.ynstr.2014.11.004
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    • "Understanding the pathophysiology of childhood ADs will provide a neuroscientific basis for novel treatment development targeting neural correlates of ADs manifesting early in life, with the potential to reduce the long-term suffering associated with the childhood onset of ADs. Animal studies have defined the neural circuit that underlies adaptive anxiety and fear responses (Aggleton and Passingham, 1981; LeDoux, 2007). The amygdala is a core component of this circuit, and numerous imaging studies link alterations in amygdala function to various forms of stress-related psychopathology (eg, Etkin and Wager, 2007; Phan et al, 2013; Stein, 2009). "
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    ABSTRACT: Children with anxiety disorders (ADs) experience persistent fear and worries that are highly debilitating, conferring risk for lifelong psychopathology. Anticipatory anxiety is a core clinical feature of childhood ADs, often leading to avoidance of uncertain and novel situations. Extensive studies in non-human animals implicate amygdala dysfunction as a critical substrate for early life anxiety. To test specific amygdala-focused hypotheses in preadolescent children with ADs, we used fMRI to characterize amygdala activation during uncertain anticipation and in response to unexpected stimuli. Forty preadolescent (age 8-12) children, 20 un-medicated AD patients and 20 matched controls, completed an anticipation task during an fMRI scan. In the task, symbolic cues preceded fear or neutral faces, such that 'certain' cues always predicted the presentation of fear or neutral faces, whereas 'uncertain' cues were equally likely to be followed by fear or neutral faces. Both AD children and controls showed robust amygdala response to faces. In response to the uncertain cues, AD children had increased amygdala activation relative to controls. Moreover, in the AD children, faces preceded by an 'uncertain' cue elicited increased amygdala activation, as compared to the same faces following a 'certain' cue. Children with ADs experience distress both in anticipation of and during novel and surprising events. Our findings suggest that increased amygdala activation may play an important role in the generation of uncertainty-related anxiety. These findings may guide the development of neuroscientifically-informed treatments aimed at relieving the suffering and preventing the lifelong disability associated with pediatric ADs.Neuropsychopharmacology accepted article preview online, 15 December 2014. doi:10.1038/npp.2014.328.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 12/2014; 40(6). DOI:10.1038/npp.2014.328 · 7.05 Impact Factor
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    • "Emotional experiences reinforce learning so that these states can be remembered and used in future behaviors. The hippocampus is known to play a critical role in the encoding and storage of episodic memories (Squire et al., 2004), whereas the amygdala is thought to enhance episodic memory storage by signaling the emotional significance of events (McGaugh, 2004; LeDoux, 2007). While studies in rodents have demonstrated enhancing effects of arousal on memory (Gallagher et al., 1977; McGaugh, 2004), human studies have suggested an emotion-induced memory trade-off, where individuals remember the central emotional content (gist) of a stimulus but often forget the details (Buchanan and Adolphs, 2002; Kensinger, 2009). "
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    ABSTRACT: Emotional arousal, mediated by the amygdala, is known to modulate episodic memories stored by the hippocampus, a region involved in pattern separation (the process by which similar representations are independently stored). While emotional modulation and pattern separation have been examined independently, the current study attempts to link the two areas of research to propose an alternative account for how emotion modulates episodic memory. We utilized an emotional discrimination task designed to tax pattern separation of emotional information by concurrently varying valence and similarity of stimuli. To examine emotional modulation of memory at the level of hippocampal subfields, we used high-resolution fMRI (1.5 mm isotropic) of the medial temporal lobe. Consistent with prior reports, we observed engagement of the hippocampal dentate gyrus (DG) and CA3 during accurate discrimination of highly similar items (i.e. pattern separation). Furthermore, we observed an emotional modulation of this signal (negative > neutral) specific to trials on which participants accurately discriminated similar emotional items. The amygdala was also modulated by emotion, regardless of the accuracy of discrimination. Additionally, we found aberrant amygdala-hippocampal network activity in a sample of adults with depressive symptoms. In this sample, amygdala activation was enhanced and DG/CA3 activation was diminished during emotional discrimination compared to those without depressive symptoms. Depressive symptom severity was also negatively correlated with DG/CA3 activity. This study suggests a novel mechanistic account for how emotional information is processed by hippocampal subfields as well as how this network may be altered in mood disorders. © 2014 Wiley Periodicals, Inc.
    Hippocampus 09/2014; 24(9). DOI:10.1002/hipo.22298 · 4.16 Impact Factor
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