<p> <b>Background:</b> Previous studies have related adverse childhood experiences (ACE) to heart disease. However, more research needs to explore neural mechanisms and psychological factors that contribute to the pathway of adverse childhood experiences leading to heart disease. <b>Purpose: </b> The present study examines racial identity as a moderator of adverse childhood experiences and cardiac autonomic dysregulation as indexed by respiratory sinus arrhythmia. <b>Method:</b> Forty-six undergraduate students of African descent attending a Historically Black University in the Mid-Atlantic region of the United States participated in this study. During the first phase, participants completed consent forms and questionnaires including the ACE Scale and the Cross Racial Identity Scale. Participants returned to the laboratory on a second occasion during which researchers employed an impedance cardiograph to record resting levels of interbeat intervals (IBI) and respiratory sinus arrhythmia (RSA). <b>Results:</b> Ordinary least squares regression analyses were conducted to test the moderating role of racial identity attitudes on the relationship between ACE prevalence and RSA. The overall regression model which included ACE prevalence, Multiculturalist attitudes, gender, and all interaction terms significantly predicted resting IBI. The overall model that included ACE prevalence, Afrocentric attitudes, gender, and all interaction terms also significantly predicted resting IBI. Participants with ACE and Afrocentric attitudes were more likely to have decreased resting RSA. Furthermore, in addition to ACE prevalence and Afrocentric attitudes, considering gender added 10% more explanatory variance in predicting resting RSA. Male participants with ACE and low Afrocentricity ratings were more likely to have decreased resting RSA. Additionally, considering gender with ACE prevalence and Miseducation attitudes added 10% more explanatory variance in predicting resting RSA. <b> Discussion:</b> Results and limitations are further discussed in the context of existing literature.</p><p>

Increasing evidence suggests that anxiety and depression disorders have neurodevelopmental roots, with a strong case for early-life serotonergic dysfunction in their ontogeny. For instance, disrupting serotonergic tone during critical developmental periods results in dysregulated adult affective behaviors, in mice. However, insight into the mechanism by which early-life serotonin levels impact emotional behaviors in later-life, remains scarce. Based on its potent neurotrophic properties, we hypothesized that serotonin acts during development to guide the maturation of brain regions implicated in the modulation of both the emotional and cognitive features of anxiety and depression disorders, namely the medial prefrontal cortex (mPFC) and hippocampus (HC). To address this hypothesis, we employed a pharmacological mouse model in which serotonin levels were increased using a selective serotonin reuptake inhibitor, fluoxetine (FLX), during a previously established critical post-natal time window (post-natal day 2-11; "PN-FLX" mouse model). The effect of this post-natal serotonergic disruption on the structural, physiological and functional properties of the adult mPFC and HC was assessed. In the mPFC, we found morphological and electrophysiological changes specific to cortical layer 2/3. Pyramidal neurons in layer 2/3 of the infralimbic (IL) sub-region of the mPFC, displayed decreased dendritic arborization, concomitant with reduced intrinsic excitability. Conversely, prelimbic (PL) layer 2/3 neurons displayed normal dendritic arborization, but increased intrinsic excitability. Together, these changes produce a reduced IL/PL output ratio. In order to probe the functional consequences of these changes, we investigated the ability of PN-FLX mice to extinguish learned fear ("fear extinction"), as performance in this behavioral paradigm is modulated by IL/PL output. Congruent with their altered IL/PL balance, PN-FLX mice display deficits in fear extinction learning and recall. Mimicking the diminished IL/PL ratio by selectively lesioning the IL, in control mice, phenocopied some features of the PN-FLX anxiety and depression-behavioral profile, demonstrating a causal relationship between mPFC changes and the emotional phenotype of PN-FLX mice. In the HC, PN-FLX treatment produced retraction of dendritic arbors but increased branching in the cornu ammonis 3 (CA3) sub-field. PN-FLX treatment also reduced total synapse number and synaptic density of CA3 neurons. In order to probe the functional consequences of these morphological changes, we investigated spatial learning in the Morris water maze and contextual fear conditioning in PN-FLX mice, as these behaviors are sensitive to CA3 manipulations. In line with reduced CA3 function, PN-FLX mice displayed deficits in both these learning paradigms. Taken together, our findings demonstrate that serotonin acts during a key developmental epoch to set the structural and physiological properties, and ultimately the functional output, of two key brain regions that underlie affective and cognitive behaviors, the mPFC and HC. Our findings provide a mechanism by which reported genetic (polymorphisms, mutations) and environmental factors (exposure to pharmacological agents or stress) that alter serotonergic tone during development, have long-term, often indelible, consequences on adult affective and cognitive function.

Functional connectivity networks that integrate remote areas of the brain as working functional units are thought to underlie fundamental mechanisms of perception and cognition, and have emerged as an active area of investigation. However, traditional approaches of measuring functional connectivity are limited in that they rely on a priori specification of one or a few brain regions. Therefore, the development of data-driven and exploratory approaches that assess functional connectivity on a large-scale are required in order to further understand the functional network organization of these processes in both health and disease. In this thesis project, I investigate the roles of functional connectivity in visual search (Chapter 2, (Pantazatos, Yanagihara et al., 2012)) and bistable perception (Chapter 3, (Karten et al., 2013)) using traditional functional connectivity approaches, and develop and apply new approaches to characterize the large-scale networks underlying the processing of supraliminal (Chapter 4, (Pantazatos et al., 2012a)) and subliminal (Chapter 5, (Pantazatos, Talati et al., 2012b)) emotional threat signals, speech and song processing in autism (Chapter 6, (Lai et al., 2012)), and face processing in social anxiety disorder (Chapter 7, (Pantazatos et al., 2013)). Finally, I complement the latter study with an investigation of structural morphological abnormalities in social anxiety disorder (Chapter 8, (Talati et al., 2013)). Each of these chapters has been or is about to be published in peer reviewed journals and this thesis provides an overview of the entire body of investigation, based on advances in understanding the role of large-scale neural processes as fundamental organizational units that underlie behavior. In Chapter 2, Independent Components Analysis (ICA), Psychophysiological Interactions (PPI) and Dynamic Causal Modeling (DCM) analyses were used to investigate the hypothesis that expectation and attention-related interactions between ventral and medial prefrontal cortex and association visual cortex underlie visual search for an object. Results extend previous models of visual search processes to include specific frontal-occipital neuronal interactions during a natural and complex search task. In Chapter 3, PPI analyses revealed percept-dependent changes in connectivity between visual cortex, frontoparietal attention and default mode networks during bistable image perception. These findings advance neural models of bistable perception by implicating the default mode and frontoparietal networks during image segmentation. In Chapters 4 and 5, an exploratory approach based on multivariate pattern analysis of large-scale, condition-dependent functional connectivity was developed and applied in order to further understand the neural mechanisms of threat-related emotion processing. This approach was successful in extracting sufficient information to "brain-read" both unattended supraliminal (Chapter 4) and subliminal (Chapter 5) fear perception in healthy subjects. Informative features for supraliminal fear perception included functional connections between thalamus and superior temporal gyrus, angular gyrus and hippocampus, and fusiform and amygdala, while informative features for subliminal fear perception included middle temporal gyrus, cerebellum and angular gyrus. In psychiatric disorders, large-scale functional connectivity is typically assessed during resting-state (i.e. no task or stimulus). However, disorder-dependent alterations in functional network architecture may be more or less prominent during a stimulus or task that is behaviorally relevant to the disorder, as is exemplified by enhanced long-range, frontal-posterior connectivity during song (vs. speech) perception in autism (Chapter 6). In the case of social anxiety disorder (SAD), pattern analysis of large-scale, functional connectivity during neutral face perception was sensitive enough to discriminate individual subjects with SAD from both healthy controls and panic disorder (Chapter 7). The most informative feature was functional connectivity between left hippocampus and left temporal pole, which was reduced in medication-free SAD subjects, and which increased following 8-weeks SSRI treatment, with greater increases correlating with greater decreases in symptom severity. This finding parallels results from observed neuroanatomical abnormalities in SAD, which include reduced grey matter volume in the temporal pole, in addition to increased grey matter volume in cerebellum and fusiform (Chapter 8). The above findings suggest promise for emerging functional connectivity and structural-based neurobiomarkers for SAD diagnosis and treatment effects.

Purpose: To better understand the relative contributions of rod, cone, and melanopsin to the human pupillary light reflex (PLR) and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief clinical protocol using the PLR. Methods: The PLR was measured with an eye tracker and stimuli controlled with a Ganzfeld system. Exp.1: 2.5-log cd/m^2 red (640±10nm) and blue (467±17nm) stimuli of various durations were presented after dark-adaptation. Exp. 2 and 3: 1-sec red and blue stimuli were presented at different intensity levels in the dark (Exp.2) or on a 0.78-log cd/m^2 blue background (Exp.3). Based on the results of Exp. 1-3, a clinical protocol was designed and tested on healthy controls (Exp. 4) and patients (Exp. 5) with retinitis pigmentosa (RP), Leber congenital amaurosis (LCA), and achmatopsia (ACHM). Results: The optimal duration for producing the melanopsin-driven sustained pupil response following termination of an intense blue stimulus was 1 sec. PLR rod- and melanopsin-driven components are best studied with low and high intensity flashes, respectively, presented in the dark (Exp. 2). A blue background suppressed rod and melanopsin responses, making it easy to assess the cone contribution with a red flash (Exp. 3). The proposed clinical protocol successfully provided reliable data from 8 normal subjects (Exp. 4). With the clinical protocol, robust melanopsin responses could be seen in the all patients with little or no contribution from the rods and cones (Exp. 5). Conclusions: It is possible to identify the rod, cone, and melanopsin contributions to the PLR with blue flashes at 2 or 3 intensity levels in dark and one red flash on a blue background.

Ambiguous motion perception occurs when an extended one-dimensional (1-D) object such as a luminance border, a line or a grating, moving behind an aperture is viewed. This ambiguity is due to the uncertainty of the veridical velocity of the moving 1-D object whose apparent velocity may vary with the change in the shape of the aperture in view. This interesting phenomenon has come to be known as the aperture problem. / In this research project, human motion perception was studied psychophysically where the geometry, number of stimulus apertures and number of moving 1-D grating components with different orientations were varied. Monocular and dichoptic viewing conditions were used to study human binocular motion processing as well. In all cases, multi-stable subjective motion percepts were observed. Specifically, when a moving 1-D stimulus was viewed behind a rectangular aperture, a unique, global, coherent motion percept or a illusory "barber pole motion" percept could be seen. An unexpected compound illusory barber pole motion percept was observed in addition to the perceived coherent motion when a cross-shaped aperture was used. The coherent motion percept and the illusory barber pole motion percepts were seen to alternate chaotically over time, with different amounts of coherent motion and component motion seen as the physical parameters of the stimuli were varied. / Multi-stable motion percepts which required binocular integration of local motion information were also observed. For example, during binocular fusion of two dichoptically viewed moving orthogonal 1-D gratings, observers could see a coherently moving unitary 2-D plaid. In addition, global coherent motion percepts also occurred with stimulation of non-overlapping visual fields stimulated separately in the two eyes. These results suggested the presence of two mechanisms, one cooperative and one competitive, operating interactively in the human visual motion channel. Furthermore, the results also support the notion that human coherent motion perception is mediately by close coupling between several putative visual channels. / Source: Dissertation Abstracts International, Volume: 52-04, Section: B, page: 2346. / Major Professor: Mark A. Berkley. / Thesis (Ph.D.)--The Florida State University, 1991.

No description available.

Evidence suggests that regions within the anterior cingulate cortex (ACC) are sensitive both to emotional and cognitive task demands. This experiment asked whether emotional and cognitive demands are processed separately by ventral and dorsal regions within the ACC, respectively. Results revealed significant individual variability between changes in anxiety and response times with practice during performance of a verb generation task. Correlational analyses of the functional magnetic resonance imaging (fMRI) data were inconclusive. However, exploratory analyses suggest that while the ventral and dorsal subdivisions of the medial prefrontal cortex, which encompasses the ACC, make specialized contributions to the processing of emotion and cognition, respectively, the two subdivisions also appear to interact. These analyses also suggest that there could be a difference in how women and men balance the competing demands of emotion and cognition that might be related to differences in self-concept and neural activity in the default mode network.

Thesis (Ph. D.)--University of Chicago, Department of Philosophy, 2002. / Includes bibliographical references. Also available on the Internet.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2009. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3793. Adviser: Arthur Kramer. Includes bibliographical references (leaves 115-148) Available on microfilm from Pro Quest Information and Learning.

<p> Individuals who are victimized by bullying during adolescence demonstrate an increased incidence of psychiatric disorders both acutely and later in life. Many of these disorders are characterized by deficits in complex cognitive functions that are mediated by the mesocortical dopamine system. The substantial maturation of the mesocortical dopamine system during adolescence may render it particularly vulnerable to insult from psychosocial stressors such as bullying. Using a rodent model of adolescent social defeat to replicate the imbalance of power inherent in teenage bullying, it was previously demonstrated that defeated rats exhibit various behavioral and neurochemical indications of mesocortical dopamine hypofunction in adulthood. The experimental chapters of this dissertation aim to further understand the consequences of victimization stress during adolescence by 1) evaluating the effects of adolescent social defeat on dopamine dependent cognitive processes and 2) investigating the potential mechanisms by which adolescent social defeat results in mesocortical dopamine hypofunction. Adult rats defeated in adolescence and their controls were initially tested on two separate tasks of working memory known to be dependent on mesocortical dopamine activity, the delayed alternating T-maze task and the delayed win-shift task. Results found a direct link between adolescent social defeat and adult working memory deficits, with previously defeated rats demonstrating impaired performance in the maintenance and utilization of information following delays of 90 seconds and 5 minutes on the T-maze and win-shift tasks respectively. In a separate experiment, quantitative autoradiography revealed increased expression of the dopamine transporter (DAT) in the infralimbic region of the medial prefrontal cortex (mPFC) of adult rats defeated in adolescence. Further investigation of mPFC DAT function utilizing <i>in vivo</i> chronoamperometry demonstrated that previously defeated rats exhibit decreased dopamine accumulation in response to pharmacological DAT inhibition, indicating enhanced DAT function that may increase clearance of dopamine in the mPFC. Combined, these results suggest that increased functional expression of DAT in the mPFC following adolescent social defeat leads to enhanced clearance of dopamine, contributing to deficits in mPFC dopamine activity and associated cognitive processes. Having identified a putative mechanism by which adolescent social defeat causes mesocortical dopamine hypofunction, the results of these experiments can assist in directing the clinical application of novel and existing pharmacotherapies to counteract the deleterious effects of adolescent stress.</p>