Laureate Institute for Brain Research

Yale, OK, United States

Laureate Institute for Brain Research

Yale, OK, United States
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Suzuki H.,Laureate Institute for Brain Research | Lucas L.R.,Rockefeller University
Cognitive, Affective and Behavioral Neuroscience | Year: 2015

Social learning theory postulates that individuals learn to engage in aggressive behavior through observing an aggressive social model. Prior studies have shown that repeatedly observing aggression, also called “chronic passive exposure to aggression,” changes accumbal dopamine D2 receptor (D2R) and amygdaloid 5-HT1B receptor (5-HT1BR) densities in observers. But, the association between these outcomes remains unknown. Thus, in our study, we used a rat paradigm to comprehensively examine the linkage between aggression, D2R density in the nucleus accumbens core (AcbC) and shell (AcbSh), and 5-HT1BR density in the medial (MeA), basomedial (BMA), and basolateral (BLA) amygdala following chronic passive exposure to aggression. Male Sprague-Dawley rats (N = 72) were passively exposed to either aggression or nonaggression acutely (1 day) or chronically (23 days). When observer rats were exposed to aggression chronically, they showed increased aggressive behavior and reduced D2R density in bilateral AcbSh. On the other hand, exposure to aggression, regardless of exposure length, increased the 5-HT1BR density in bilateral BLA. Finally, low D2R in the AcbSh significantly interacted with high 5-HT1BR density in the BLA to predict high levels of aggression in observer rats. Our results advance our understanding of the neurobiological mechanisms in the observational learning of aggression, highlighting that dopamine–serotonin interaction, or AcbSh–BLA interaction, may contribute to a risk factor for aggression in observers who chronically witness aggressive interactions. © 2015, Psychonomic Society, Inc.


Savitz J.B.,Laureate Institute for Brain Research | Drevets W.C.,Laureate Institute for Brain Research | Drevets W.C.,University of Oklahoma
Neurobiology of Disease | Year: 2013

The in vivo study of receptor binding potential in the human brain is made possible by positron emission tomography (PET) imaging. Here we review PET studies of neuroreceptor function in mood disorders - specifically, major depressive disorder (MDD) and bipolar disorder (BD). We concentrate on the most widely studied receptors of the serotonergic and dopaminergic systems. Specifically, the serotonin 1A (5-HT1A), serotonin 2A (5-HT2A), serotonin 1B (5-HT1B), dopamine 1 (D1), and dopamine 2/3 (D2/3) receptors. We also review PET studies of the serotonin transporter (5-HTT), the dopamine transporter (DAT), monoamine oxidase A (MAO-A), and the muscarinic 2 receptor (M2). On the basis of the PET literature as well as supporting genetic studies, postmortem data, and preclinical models of depression, and several models of how monoaminergic function is altered in mood disorders are discussed with respect to inflammation, endocrine dysfunction, depression subtypes, and altered neurocircuitry. © 2012 Elsevier Inc.


Murray E.A.,U.S. National Institutes of Health | Wise S.P.,Olschefskie Institute for the Neurobiology of Knowledge | Drevets W.C.,Laureate Institute for Brain Research | Drevets W.C.,University of Oklahoma
Biological Psychiatry | Year: 2011

Despite considerable effort, the localization of dysfunction in major depressive disorder (MDD) remains poorly understood. We present a hypothesis about its localization that builds on recent findings from primate neuropsychology. The hypothesis has four key components: a deficit in the valuation of "self" underlies the core disorder in MDD; the medial frontal cortex represents "self"; interactions between the amygdala and cortical representations update their valuation; and inefficiency in using positive feedback by orbital prefrontal cortex contributes to MDD. © 2011 Society of Biological Psychiatry.


Barrett L.F.,Northeastern University | Barrett L.F.,Massachusetts General Hospital | Simmons W.K.,Laureate Institute for Brain Research | Simmons W.K.,University of Tulsa
Nature Reviews Neuroscience | Year: 2015

Intuition suggests that perception follows sensation and therefore bodily feelings originate in the body. However, recent evidence goes against this logic: interoceptive experience may largely reflect limbic predictions about the expected state of the body that are constrained by ascending visceral sensations. In this Opinion article, we introduce the Embodied Predictive Interoception Coding model, which integrates an anatomical model of corticocortical connections with Bayesian active inference principles, to propose that agranular visceromotor cortices contribute to interoception by issuing interoceptive predictions. We then discuss how disruptions in interoceptive predictions could function as a common vulnerability for mental and physical illness. © 2015 Macmillan Publishers Limited.


Yuan H.,Laureate Institute for Brain Research | He B.,University of Minnesota
IEEE Transactions on Biomedical Engineering | Year: 2014

Many studies over the past two decades have shown that people can use brain signals to convey their intent to a computer using brain-computer interfaces (BCIs). BCI systems extract specific features of brain activity and translate them into control signals that drive an output. Recently, a category of BCIs that are built on the rhythmic activity recorded over the sensorimotor cortex, i.e., the sensorimotor rhythm (SMR), has attracted considerable attention among the BCIs that use noninvasive neural recordings, e.g., electroencephalography (EEG), and have demonstrated the capability of multidimensional prosthesis control. This paper reviews the current state and future perspectives of SMR-based BCI and its clinical applications, in particular focusing on the EEG SMR. The characteristic features of SMR from the human brain are described and their underlying neural sources are discussed. The functional components of SMR-based BCI, together with its current clinical applications, are reviewed. Finally, limitations of SMR-BCIs and future outlooks are also discussed. © 1964-2012 IEEE.


Inflammation-related changes in the concentrations of kynurenine pathway metabolites occur in depression secondary to medical conditions but are not firmly established in primary mood disorders. Reductions in hippocampal and amygdalar volume that putatively reflect dendritic atrophy are widely reported in major depressive disorder (MDD). Here we tested whether the relative serum concentrations of putatively neuroprotective (kynurenic acid (KA)) and neurotoxic (3-hydroxykynurenine (3HK) and quinolinic acid (QA)) kynurenine pathway metabolites were altered in primary MDD and whether these metabolites were associated with hippocampal and amygdalar volume. A total of 29 moderately to severely depressed unmedicated subjects who met DSM-IV criteria for MDD and 20 healthy controls (HCs) completed a structural MRI scan and provided blood sample for kynurenine metabolite analysis, performed using high-performance liquid chromatography with tandem mass spectrometry. Cytokine concentrations were measured with ELISA and gray matter volumes were measured with the automated segmentation software, FreeSurfer. An a priori defined variable of interest, the KA/QA ratio, a putative neuroprotective index, trended lower in the MDD versus the HC group and correlated negatively with anhedonia but positively with the total hippocampal and amygdala volume in the MDD subjects. The post hoc data reduction methods yielded three principal components. Component 1 (interleukin-1 receptor antagonist, QA, and kynurenine) was significantly elevated in MDD participants versus the HCs, whereas component 2 (KA, tryptophan, and kynurenine) was positively correlated with hippocampal and amygdala volume within the MDD group. Our results raise the possibility that an immune-related imbalance in the relative metabolism of KA and QA predisposes to depression-associated dendritic atrophy and anhedonia.Neuropsychopharmacology advance online publication, 27 August 2014; doi:10.1038/npp.2014.194.


Ding L.,University of Oklahoma | Yuan H.,Laureate Institute for Brain Research
Human Brain Mapping | Year: 2013

Electroencephalography (EEG) and magnetoencephalography (MEG) have different sensitivities to differently configured brain activations, making them complimentary in providing independent information for better detection and inverse reconstruction of brain sources. In the present study, we developed an integrative approach, which integrates a novel sparse electromagnetic source imaging method, i.e., variation-based cortical current density (VB-SCCD), together with the combined use of EEG and MEG data in reconstructing complex brain activity. To perform simultaneous analysis of multimodal data, we proposed to normalize EEG and MEG signals according to their individual noise levels to create unit-free measures. Our Monte Carlo simulations demonstrated that this integrative approach is capable of reconstructing complex cortical brain activations (up to 10 simultaneously activated and randomly located sources). Results from experimental data showed that complex brain activations evoked in a face recognition task were successfully reconstructed using the integrative approach, which were consistent with other research findings and validated by independent data from functional magnetic resonance imaging using the same stimulus protocol. Reconstructed cortical brain activations from both simulations and experimental data provided precise source localizations as well as accurate spatial extents of localized sources. In comparison with studies using EEG or MEG alone, the performance of cortical source reconstructions using combined EEG and MEG was significantly improved. We demonstrated that this new sparse ESI methodology with integrated analysis of EEG and MEG data could accurately probe spatiotemporal processes of complex human brain activations. This is promising for noninvasively studying large-scale brain networks of high clinical and scientific significance. Hum Brain Mapp, 2013. © 2010 Wiley Periodicals, Inc. Copyright © 2011 Wiley Periodicals, Inc..


Avery J.A.,Laureate Institute for Brain Research
Neuropsychopharmacology | Year: 2016

Discontinuing unhealthy behaviors, such as overeating or drug use, depends upon an individual’s ability to overcome the influence of environmental reward cues. The strength of that influence, however, varies greatly depending upon the internal state of the body. Characterizing the relationship between interoceptive signaling and shifting drug cue valuation provides an opportunity for understanding the neural bases of how changing internal states alter reward processing more generally. A total of 17 cigarette smokers rated the pleasantness of cigarette pictures when they were nicotine sated or nicotine abstinent. On both occasions, smokers also underwent functional magnetic resonance imaging (fMRI) scanning while performing a visceral interoceptive attention task and a resting-state functional connectivity scan. Hemodynamic, physiological, and behavioral parameters were compared between sated and abstinent scans. The relationships between changes in these parameters across scan sessions were also examined. Smokers rated cigarette pictures as significantly more pleasant while nicotine abstinent than while nicotine sated. Comparing abstinent with sated scans, smokers also exhibited significantly decreased mid-insula, amygdala, and orbitofrontal activity while attending to interoceptive signals from the body. Change in interoceptive activity within the left mid-insula predicted the increase in smoker’s pleasantness ratings of cigarette cues. This increase in pleasantness ratings was also correlated with an increase in resting-state functional connectivity between the mid-insula and the ventral striatum and ventral pallidum. These findings support a model wherein interoceptive processing in the mid-insula of withdrawal signals from the body potentiates the motivational salience of reward cues through the recruitment of hedonic ‘hot spots’ within the brain’s reward circuitry.Neuropsychopharmacology advance online publication, 17 August 2016; doi:10.1038/npp.2016.128. © 2016 American College of Neuropsychopharmacology


News Article | November 15, 2016
Site: www.businesswire.com

SALT LAKE CITY--(BUSINESS WIRE)--Laureate Institute for Brain Research (LIBR) has developed an integration between its Ceph clustered file system storage environment and the Spectra® BlackPearl® Deep Storage Gateway.


News Article | March 22, 2016
Site: www.sciencenews.org

In a pair of twin sisters, a rare disease had damaged the brain’s structures believed necessary to feel fear. But an injection of a drug could nevertheless make them anxious. The results of that experiment, described in the March 23 Journal of Neuroscience, add to evidence that the amygdalae, small, almond-shaped brain structures tucked deep in the brain, aren’t the only bits of the brain that make a person feel afraid. “Overall, this suggests multiple different routes in the brain to a common endpoint of the experience of fear,” says cognitive neuroscientist Stephan Hamann of Emory University in Atlanta. The twins, called B.G. and A.M., have Urbach-Wiethe disease, a genetic disorder that destroyed most of their amygdalae in late childhood. Despite this, the twins showed fear after inhaling air laden with extra carbon dioxide (an experience that can create the sensation of suffocating), an earlier study showed (SN: 3/23/13, p. 12). Because carbon dioxide affects a wide swath of the body and brain, scientists turned to a more specific cause of fear that stems from inside the body: a drug called isoproterenol, which can set the heart racing and make breathing hard. Sensing these bodily changes provoked by the drug can cause anxiety. “If you know what adrenaline feels like, you know what isoproterenol feels like,” says study coauthor Sahib Khalsa, a psychiatrist and neuroscientist at the Laureate Institute for Brain Research in Tulsa, Okla. After injections of isoproterenol, both twins felt shaky and anxious. B.G. experienced a full-blown panic attack, a result of the drug that afflicts about a quarter of people who receive it, says Khalsa. In a second experiment, researchers tested the women’s ability to judge their bodies’ responses to the drug. While receiving escalating doses, the women rated the intensity of their heartbeats and breathing. A.M., the woman who didn’t have a panic attack, was less accurate at sensing the drug’s effects on her body than both her sister and healthy people, researchers found. It’s not clear why the twins responded differently, Khalsa says. Further experiments using brain scans may help pinpoint neural differences that could be behind the different reactions. The results suggest that the amygdala isn’t the only part of the brain involved in fear and anxiety, but there’s more work to do before scientists understand how the brain creates these emotions, Khalsa says. “It’s definitely a complicated question and a debate that’s unresolved,” he says.

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