Alexander Shackman
The broad aim of my laboratory’s multi-disciplinary research program is to identify and understand the mechanisms that contribute to the development of anxiety and mood disorders. Consistent with the NIMH Strategic Objectives and Research Domain Criteria (RDoC) initiative, most of our work is focused on identifying the neural basis of trait-like individual differences in anxiety and neuroticism, important prospective risk factors for the development of internalizing psychopathology and co-morbid substance abuse. Over the past decade, we have used a combination of multimodal brain imaging (MRI/PET), electrophysiology (EEG/ERP), peripheral physiology (cortisol, fear-potentiated startle), behavioral assays, and clinical assessments to address three central questions:
1) What neural mechanisms confer increased risk for developing anxiety and depression?
• Leveraging large biobehavioral datasets, our recent work highlights the important contribution of individual differences in the activity and functional architecture of networks encompassing the extended amygdala, prefrontal cortex, and cingulate cortex (e.g., Nusslock, Shackman, Coan, Harmon-Jones, Alloy & Abramson J Abnorm Psychol 2011; Shackman et al. PNAS USA 2013 and Psychol Sci 2009; Birn, Shackman et al. Mol Psychiatry, 2014; Roseboom et al. Biol Psychiatry in press). Active collaborations with L Pessoa, NA Fox, NH Kalin (Wisconsin), JJ Curtin (Wisconsin), RJ Davidson (Wisconsin), RM Birn (Wisconsin), T Hendler (Tel Aviv), and L Somerville (Harvard). More recently, our laboratory has established mobile phone-based techniques for ecological momentary assessment (EMA). EMA provides a unique opportunity to clarify the real-world significance of artificial laboratory measures of brain function and to identify the maladaptive behavioral pathways that link heightened dispositional anxiety to dysfunction and psychopathology.
2) How does dispositional anxiety influence on-going thoughts, feelings, and behavior?
• Using a combination of emotional face stimuli and threat-of-shock, our recent work demonstrates that anxious individuals allocate excess attention and working memory to threat in the lab. This bias is potentiated by stress and enables threat-related information to influence on-going thoughts, feelings, and behavior in ways that likely promote psychopathology (Stout, Shackman et al. Frontiers Hum Neurosci 2013; Shackman et al. J Neurosci 2011 and Emotion 2006, 2007). Active collaborations with L Pessoa, M Gamer, SD Pollak (Wisconsin), and CL Larson (UW-Milwaukee)
3) What neural mechanisms underlie anxious individuals’ inhibited, avoidant behavior?
• Our work underscores the role of individual differences in a cingulate-centered circuit that plays a key role in governing the passive and active avoidance of threat (Shackman et al. Nature Reviews Neurosci 2011 and Cavanagh & Shackman J Physiol Paris in press). Active collaborations with L Pessoa and DA Seminowicz (UMB School of Dentistry).
Collectively, this work has provided important new insights into the mechanisms underlying the risk to develop a range of common neuropsychiatric disorders and sets the stage for accelerated development of more effective, personalized, and neurobiologically-grounded prevention and treatment strategies. From a basic psychological science perspective, our work starts to address fundamental questions about the nature of personality and the interplay of emotion and cognition.
Techniques
Multimodal neuroimaging (event-related and resting-state fMRI, PET, VBM); Peripheral physiology (cortisol, facial EMG, fear-potentiated startle); Electrophysiology (ERP/EEG, LORETA source modeling); Quantitative methods, especially the application of multivariate techniques and classical psychometrics to imaging and ERP measures; meta-analysis (ALE, random-effects).
Research Interests
Affective and cognitive neuroscience; neural bases of threat processing, anxiety, and their application to psychiatric disorders; neural bases of personality and individual differences in state/trait anxiety and behavioral inhibition; cognition × emotion interactions: interactions of anxiety and higher cognition (cognitive control, selective attention, and working memory); amygdala; prefrontal cortex; cingulate cortex.
Address: Department of Psychology & Maryland Neuroimaging Center
University of Maryland
1147 Biology/Psychology Building
College Park, MD 20742
1) What neural mechanisms confer increased risk for developing anxiety and depression?
• Leveraging large biobehavioral datasets, our recent work highlights the important contribution of individual differences in the activity and functional architecture of networks encompassing the extended amygdala, prefrontal cortex, and cingulate cortex (e.g., Nusslock, Shackman, Coan, Harmon-Jones, Alloy & Abramson J Abnorm Psychol 2011; Shackman et al. PNAS USA 2013 and Psychol Sci 2009; Birn, Shackman et al. Mol Psychiatry, 2014; Roseboom et al. Biol Psychiatry in press). Active collaborations with L Pessoa, NA Fox, NH Kalin (Wisconsin), JJ Curtin (Wisconsin), RJ Davidson (Wisconsin), RM Birn (Wisconsin), T Hendler (Tel Aviv), and L Somerville (Harvard). More recently, our laboratory has established mobile phone-based techniques for ecological momentary assessment (EMA). EMA provides a unique opportunity to clarify the real-world significance of artificial laboratory measures of brain function and to identify the maladaptive behavioral pathways that link heightened dispositional anxiety to dysfunction and psychopathology.
2) How does dispositional anxiety influence on-going thoughts, feelings, and behavior?
• Using a combination of emotional face stimuli and threat-of-shock, our recent work demonstrates that anxious individuals allocate excess attention and working memory to threat in the lab. This bias is potentiated by stress and enables threat-related information to influence on-going thoughts, feelings, and behavior in ways that likely promote psychopathology (Stout, Shackman et al. Frontiers Hum Neurosci 2013; Shackman et al. J Neurosci 2011 and Emotion 2006, 2007). Active collaborations with L Pessoa, M Gamer, SD Pollak (Wisconsin), and CL Larson (UW-Milwaukee)
3) What neural mechanisms underlie anxious individuals’ inhibited, avoidant behavior?
• Our work underscores the role of individual differences in a cingulate-centered circuit that plays a key role in governing the passive and active avoidance of threat (Shackman et al. Nature Reviews Neurosci 2011 and Cavanagh & Shackman J Physiol Paris in press). Active collaborations with L Pessoa and DA Seminowicz (UMB School of Dentistry).
Collectively, this work has provided important new insights into the mechanisms underlying the risk to develop a range of common neuropsychiatric disorders and sets the stage for accelerated development of more effective, personalized, and neurobiologically-grounded prevention and treatment strategies. From a basic psychological science perspective, our work starts to address fundamental questions about the nature of personality and the interplay of emotion and cognition.
Techniques
Multimodal neuroimaging (event-related and resting-state fMRI, PET, VBM); Peripheral physiology (cortisol, facial EMG, fear-potentiated startle); Electrophysiology (ERP/EEG, LORETA source modeling); Quantitative methods, especially the application of multivariate techniques and classical psychometrics to imaging and ERP measures; meta-analysis (ALE, random-effects).
Research Interests
Affective and cognitive neuroscience; neural bases of threat processing, anxiety, and their application to psychiatric disorders; neural bases of personality and individual differences in state/trait anxiety and behavioral inhibition; cognition × emotion interactions: interactions of anxiety and higher cognition (cognitive control, selective attention, and working memory); amygdala; prefrontal cortex; cingulate cortex.
Address: Department of Psychology & Maryland Neuroimaging Center
University of Maryland
1147 Biology/Psychology Building
College Park, MD 20742
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Papers by Alexander Shackman
(BNST), two nuclei within the central extended amygdala, function as critical relays
within the distributed neural networks that coordinate sensory, emotional, and cognitive
responses to threat. These structures have overlapping anatomical projections to
downstream targets that initiate defensive responses. Despite these commonalities,
researchers have also proposed a functional dissociation between the CeA and BNST,
with the CeA promoting responses to discrete stimuli and the BNST promoting
responses to diffuse threat. Intrinsic functional connectivity (iFC) provides a means to
investigate the functional architecture of the brain, unbiased by task demands. Using
ultra-high field neuroimaging (7-Tesla fMRI), which provides increased spatial resolution, this study compared the iFC networks of the CeA and BNST in 27 healthy individuals. Both structures were coupled with areas of the medial prefrontal cortex, hippocampus, thalamus, and periaqueductal gray matter. Compared to the BNST, the bilateral CeA was more strongly coupled with the insula and regions that support sensory processing, including thalamus and fusiform gyrus. In contrast, the bilateral BNST was more strongly coupled with regions involved in cognitive and motivational processes, including the dorsal paracingulate gyrus, posterior cingulate cortex, and striatum. Collectively, these findings suggest that responses to sensory stimulation are preferentially coordinated by the CeA and cognitive and motivational responses are preferentially coordinated by the BNST.
(BNST), two nuclei within the central extended amygdala, function as critical relays
within the distributed neural networks that coordinate sensory, emotional, and cognitive
responses to threat. These structures have overlapping anatomical projections to
downstream targets that initiate defensive responses. Despite these commonalities,
researchers have also proposed a functional dissociation between the CeA and BNST,
with the CeA promoting responses to discrete stimuli and the BNST promoting
responses to diffuse threat. Intrinsic functional connectivity (iFC) provides a means to
investigate the functional architecture of the brain, unbiased by task demands. Using
ultra-high field neuroimaging (7-Tesla fMRI), which provides increased spatial resolution, this study compared the iFC networks of the CeA and BNST in 27 healthy individuals. Both structures were coupled with areas of the medial prefrontal cortex, hippocampus, thalamus, and periaqueductal gray matter. Compared to the BNST, the bilateral CeA was more strongly coupled with the insula and regions that support sensory processing, including thalamus and fusiform gyrus. In contrast, the bilateral BNST was more strongly coupled with regions involved in cognitive and motivational processes, including the dorsal paracingulate gyrus, posterior cingulate cortex, and striatum. Collectively, these findings suggest that responses to sensory stimulation are preferentially coordinated by the CeA and cognitive and motivational responses are preferentially coordinated by the BNST.