Article

Hamann S, Mao H. Positive and negative emotional verbal stimuli elicit activity in the left amygdala. NeuroReport 13: 15-19

Department of Psychology, Emory University, Atlanta, Georgia, United States
Neuroreport (Impact Factor: 1.52). 02/2002; 13(1):15-9. DOI: 10.1097/00001756-200201210-00008
Source: PubMed

ABSTRACT

The human amygdala's involvement in negative emotion is well established, but relatively little is known regarding its role in positive emotion. Here we examined the neural response to emotionally positive, negative, and neutral words using fMRI. Relative to neutral words, positive and negative emotional words elicited greater activity in the left amygdala. Positive but not negative words elicited activity in dorsal and ventral striatal regions which have been linked in previous neuroimaging studies to reward and positive affect, including caudate, putamen, globus pallidus, and accumbens. These findings provide the first direct evidence that the amygdala is involved in emotional reactions elicited by both positive and negative emotional words, and further indicate that positive words additionally activate brain regions related to reward.

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    • ", 2000 ; Tabert et al . , 2001 ; Hamann and Mao , 2002 ; Cunningham et al . , 2004 ; Herbert et al . "
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    ABSTRACT: Persons suffering from anxiety disorders display facilitated processing of arousing and negative stimuli, such as negative words. This memory bias is reflected in better recall and increased amygdala activity in response to such stimuli. However, individual learning histories were not considered in most studies, a concern that we meet here. Thirty-four female persons (half with high-, half with low trait anxiety) participated in a criterion-based associative word-learning paradigm, in which neutral pseudowords were paired with aversive or neutral pictures, which should lead to a valence change for the negatively paired pseudowords. After learning, pseudowords were tested with fMRI to investigate differential brain activation of the amygdala evoked by the newly acquired valence. Explicit and implicit memory was assessed directly after training and in three follow-ups at 4-day intervals. The behavioral results demonstrate that associative word-learning leads to an explicit (but no implicit) memory bias for negatively linked pseudowords, relative to neutral ones, which confirms earlier studies. Bilateral amygdala activation underlines the behavioral effect: Higher trait anxiety is correlated with stronger amygdala activation for negatively linked pseudowords than for neutrally linked ones. Most interestingly, this effect is also present for negatively paired pseudowords that participants could not remember well. Moreover, neutrally paired pseudowords evoked higher amygdala reactivity than completely novel ones in highly anxious persons, which can be taken as evidence for generalization. These findings demonstrate that few word-learning trials generate a memory bias for emotional stimuli, indexed both behaviorally and neurophysiologically. Importantly, the typical memory bias for emotional stimuli and the generalization to neutral ones is larger in high anxious persons.
    Full-text · Article · Sep 2015 · Frontiers in Psychology
    • "Yet another meta-analysis found both hypo-and hyperactivation in the striatum in depression with valence-specific findings (Groenewold et al., 2012). In healthy participants, the research is also mixed, with some studies demonstrating striatal reactivity to positive, but not negative, conditions (Hamann and Mao, 2002; Hare et al., 2005), and others indicating greater striatal activation in response to unpleasant compared with pleasant or neutral stimuli (Carretie et al., 2009). It is unclear, at this point, if the striatum responds to specific valence conditions in a similar pattern in depressed participants compared with healthy participants. "
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    ABSTRACT: The extent to which affective reactivity and associated neural underpinnings are altered by depression remains equivocal. This study assessed striatal activation in fifty-one unmedicated female participants meeting DSM-IV criteria for Major Depressive Disorder (MDD) and 61 age-matched healthy females (HC) aged 17-63 years. Participants completed an affective reactivity functional magnetic resonance imaging task. Data were preprocessed using SPM8, and region-of-interest analyses were completed using MarsBaR to extract caudate, putamen, and nucleus accumbens (NAcc) activation. General linear repeated measure ANOVAs were used to assess group differences and correlational analyses were used to measure the association between activation, depression severity, and anhedonia. Main effects of hemisphere, valence, and group status were observed, with MDD participants demonstrating decreased striatal activation compared with HC. Across groups and valence types, the left hemisphere demonstrated greater activation than the right hemisphere in the putamen and nucleus accumbens, whereas the right hemisphere demonstrated greater activation than the left in the caudate. Additionally, unpleasant stimuli elicited greater activation than pleasant and neutral stimuli in the caudate and putamen, and unpleasant stimuli elicited greater activation than neutral stimuli in the NAcc. There were no significant associations between activation, depression severity, and anhedonia. Overall, depression was characterized by reduced affective reactivity in the striatum, regardless of stimuli valence, supporting the emotion context insensitivity model of depression. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · May 2015 · Journal of Psychiatric Research
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    • "The human amygdala mediates interaction between the body and the brain during affective processing. The amygdala supports the perception of fear signals and threat (Zald, 2003; Phelps and LeDoux, 2005) and its activity correlates with emotional intensity rating of affective pictures (Phan et al., 2004), including facial expressions (Hamann and Mao, 2002). "
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    ABSTRACT: Autonomic nervous system activity is an important component of human emotion. Mental processes influence bodily physiology, which in turn feeds back to influence thoughts and feelings. Afferent cardiovascular signals from arterial baroreceptors in the carotid sinuses are processed within the brain and contribute to this two-way communication with the body. These carotid baroreceptors can be stimulated non-invasively by externally applying focal negative pressure bilaterally to the neck. In an experiment combining functional neuroimaging (fMRI) with carotid stimulation in healthy participants, we tested the hypothesis that manipulating afferent cardiovascular signals alters the central processing of emotional information (fearful and neutral facial expressions). Carotid stimulation, compared to sham stimulation, broadly attenuated activity across cortical and brainstem regions. Modulation of emotional processing was apparent as a significant expression-by-stimulation interaction within left amygdala, where responses during appraisal of fearful faces were selectively reduced by carotid stimulation. Moreover, activity reductions within insula, amygdala, and hippocampus correlated with the degree of stimulation-evoked change in the explicit emotional ratings of fearful faces. Across participants, individual differences in autonomic state (heart rate variability, a proxy measure of autonomic balance toward parasympathetic activity) predicted the extent to which carotid stimulation influenced neural (amygdala) responses during appraisal and subjective rating of fearful faces. Together our results provide mechanistic insight into the visceral component of emotion by identifying the neural substrates mediating cardiovascular influences on the processing of fear signals, potentially implicating central baroreflex mechanisms as for anxiolytic treatment targets.Neuropsychopharmacology accepted article preview online, 12 January 2015. doi:10.1038/npp.2015.10.
    Full-text · Article · Jan 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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