The current study examined the effects of kangaroo care on breastfeeding practices, infant stress reactivity, and biobehavioral measures of mother-infant bonding across the first 3 months postpartum. Additionally, the role of breastfeeding in infant cortical maturation in the frontal lobe was examined. Thirty two mother-infant dyads participated in the current study; 16 mother-infant dyads were randomly assigned to the kangaroo care group and 17 mother-infant dyads were assigned to the control group. Mothers in the kangaroo care group received training on proper kangaroo care procedures by a trained administrator during the first 1-2 weeks postpartum. Mothers in the kangaroo care group were asked to use the kangaroo care procedure for 1 hour per day for 6 weeks. Maternal perceptions of fetal attachment, mood, feeding intentions, and urinary oxytocin measurements were assessed prenatally. At a newborn visit, infant neurobehavioral functioning and urinary oxytocin measurements were assessed. Maternal mood and feeding practices were also assessed at the newborn visit. At 3 months postpartum, mother-infant dyads were assessed on urinary oxytocin measurements. Mother-infant dyads were recorded during a play session and feeding session. Infant baseline EEG recordings were taken over a 5 minute period. Infant cortisol measurements were collected from infant saliva before and after a mild behavioral stressor, an infant arm restraint procedure. Maternal perceptions of postpartum bonding, mood, infant temperament, and feeding practices were also assessed. Results indicate that kangaroo care produced medium to large effects on cortisol reactivity, dyadic bonding, and breastfeeding practices if kangaroo care was practiced for the recommended amount of time. Kangaroo care produced medium to large effects on oxytocin levels in motherinfant dyads regardless of use. Cortical measures of infant frontal activity indicated that all infants in the samples displayed functional maturity of the frontal lobe. Kangaroo care can be used a viable, low-cost tactile procedure that can be implemented after birth to aid in breastfeeding practices, mother-infant bonding, and lower infant stress reactivity. Infants in the study who received at least one breastfeeding session displayed advanced patterns of frontal activation. Further study is needed to determine if peripheral oxytocin measurements are 1) reliable and 2) are indicative of dyadic bonding behaviors. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2014. / FAU Electronic Theses and Dissertations Collection

From locating a secure home, foraging for food, running away from predators, spatial navigation is an integral part of everyday life. Multiple brain regions work together to form a three-dimensional representation of our environment; specifically, place cells, grid cells, border cells & head direction cells are thought to interact and influence one another to form this cognitive map. Head direction (HD) cells fire as the animal moves through space, according to directional orientation of the animal’s head with respect to the laboratory reference frame, and are therefore considered to represent the directional sense. Interestingly, inactivation of head direction cell-containing brain regions has mixed consequences on spatial behavior. Current methods of identifying HD cells are limited to in vivo electrophysiological recordings in a dry-land environment. We first developed a dry-land version of the MWM in order to carry out behavioral-recording paired studies. Additionally, to learn about HD cells function we quantified expression of neuronal activation marker (c-Fos), and L-amino acid transporter 4 (Lat4) in neurons found within the HD cell dense anterodorsal thalamic nucleus (ADN) in mice after exploratory behavior in an open field, or forward unidirectional movement on a treadmill. We hypothesize that the degree to which ADN neurons are activated during exploratory behavior is influenced by the range of heading directions sampled. Additionally, we hypothesize that c-Fos and Lat4 are colocalized within ADN neurons following varying amounts of head direction exposure. Results indicate that following free locomotion of mice in an open field arena, which permitted access to 360° of heading, a greater number of ADN neurons express c-Fos protein compared to those exposed to a limited range of head directions during locomotion in a treadmill. These findings suggest that the degree of ADN neuronal activation was dependent upon the range of head directions sampled. We observed a high degree of colocalization of c-Fos and Lat4 within ADN suggesting that Lat4 may be a useful tool to manipulate neuronal activity of HD cells. Identifying genetic markers specific to ADN helps provide an essential understanding of the spatial navigation system, and supports development of therapies for cognitive disorders affecting navigation. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2017. / FAU Electronic Theses and Dissertations Collection

abstract: The present series of studies examined whether a novel implementation of an intermittent restraint (IR) chronic stress paradigm could be used to investigate hippocampal-dependent spatial ability in both sexes. In experiments 1 and 2, Sprague- Dawley male rats were used to identify the optimal IR parameters to assess spatial ability. For IR, rats were restrained for 2 or 6hrs/day (IR2, IR6, respectively) for five days and then given two days off, a process that was repeated for three weeks and compared to rats restrained for 6hrs/d for each day (DR6) and non-stressed controls (CON). Spatial memory was tested on the radial arm water maze (RAWM), object placement (OP), novel object recognition (NOR) and Y-maze. The results for the first two experiments revealed that IR6, but not IR2, was effective in impairing spatial memory in male rats and that task order impacted performance. In experiment 3, an extended IR paradigm for six weeks was implemented before spatial memory testing commenced in male and female rats (IR- M, IR-F). Unexpectedly, an extended IR paradigm failed to impair spatial memory in either males or females, suggesting that when extended, the IR paradigm may have become predictable. In experiment 4, an unpredictable IR (UIR) paradigm was implemented, in which restraint duration (30 or 60-min) combined with orbital shaking, time of day, and the days off from UIR were varied. UIR impaired spatial memory in males, but not females. Together with other reports, these findings support the interpretation that chronic stress negatively impairs hippocampal-dependent function in males, but not females, and that females appear to be resilient to spatial memory deficits in the face of chronic stress. / Dissertation/Thesis / Masters Thesis Psychology 2019

Bacteria in the gastrointestinal tract play an important role in intestinal motility, inflammation, homeostasis, and behavior. Bacteria, through the natural synthesis of neuroactive compounds and secondary metabolites, can modulate the host immune system and communicate with the host along the signaling pathway along the gut-brain axis. Here, we functionally design, develop, test, and characterize a platform for the study of microbial-host interactions using advancements in the field of synthetic biology. First, we describe the engineering of Escherichia coli Nissle to biosynthesize serotonin within the mammalian gut using a native-plasmid optimized approach. Serotonin is crucial for neurotransmission throughout the body and may be playing a role in microbial gut-brain communication. In the gastrointestinal tract, serotonin regulates intestinal motility, cell turnover, intestinal inflammation, and gastrointestinal homeostasis. Upon serial daily oral gavages, our engineered bacterium populates a murine colon to produce serotonin locally in the mucosa layers along the epithelial lining. Changes in host physiology were observed including decreased gastrointestinal motility, increased colonic Muc2 expression, induction of host TPH2, responsible for serotonin biosynthesis in enteric neurons, and upregulation of serotonin receptors HTR3, HTR4, and HTR7 in the colon. Behavioral tests revealed a statistically significant decrease in anxiety and depression in stress-induced environments in mice treated with the engineered bacterium. This work suggests that gut bacteria engineered to modulate host gut-brain axis may have both scientific and clinical uses to study microbial-host interactions and treat gastrointestinal and behavioral mood disorders in humans. Second, we engineered bacteria to produce exogenous butyrate and other SCFAs in the murine gut. Short chain fatty acids (SCFAs) play an important role in intestinal homeostasis, fluid dynamics, inflammation, oxidative stress, and intestinal hypersensitivity and motility. With this development, we characterized the effects of our butyrate-producing bacteria on a high-fat diet and DSS-induced colitis model within the colon. Although energetically burdensome to produce, our strains produced butyrate in the colon at higher density in an actively inflamed colitis model. After 14 days of oral administration, our engineered strain (EcN:B) increased the colon length of normal wild-type mice, in high fat fed mice, and in mice with recovering and actively inflamed DSS-induced colitis. EcN:B increased mucosal barrier thickness, upregulated gene expression of the barrier integrity markers Cldn1, Ocln, Zo1, and altered crypt and villus height during inflammation recovery. Furthermore, as butyrate is known to induce Foxp3+ Regulatory T cells, we saw a 13.01% percent increase in Foxp3+ cells in the colon of mice fed our engineered bacteria. This work suggests that synthetic gut bacteria engineered to produce short chain fatty acids may have future clinical uses to treat patients with inflammatory bowel disease including Crohn’s and Colitis with future potential to serve as a therapeutic for irritable bowel syndrome, idiopathic constipation, obesity, and colorectal cancer. This platform, with the use of synthetic biology to natively engineer Escherichia coli Nissle to produce bioactive compounds in the distal gastrointestinal tract, creates a framework for future characterization of bacterial-host communication and future microbial-based therapeutics.

This dissertation evaluates preksha dhyana, a form of modern yoga introduced by the Jain Shvetambara Terapanth in 1975. Modern yoga emerged as a consequence of a complex encounter of Indian yogic gurus, American and British metaphysical thinkers, and modern ideas about science and health. I provide a brief history of the Terapanth from its eighteenth-century founder, Bikshu, to its current monastic guru, Mahaprajna, who constructed preksha dhyana. I evaluate the historical trajectory that led from the Terapanth's beginnings as a sect that maintained a world-rejecting ascetic ideal to its late twentieth-century introduction of preksha dhyana, which is popularly disseminated as a practice aimed at health and well-being. The practice and ideology of preksha dhyana is, however, context specific. In the Terapanthi monastic context, it functions as a metaphysical, mystical, and ascetic practice. In this way, it intersects with classical schools of yoga, which aim at ascetic purification and release from the world. In its popular dissemination by the samanis, female members of an intermediary Terapanthi monastic order, it functions as a physiotherapeutic practice. The samanis teach yoga to students in India, the United States, and Britain whose interests are primarily in yoga's physical and psychological benefits. In this way, it is a case study of modern yoga, which aims at the enhancement of the body and life in the world. I demonstrate how the samanis are mediators of their guru, Mahaprajna, and thus resolve ancient and contemporary tensions between ascetic and worldly values. I also demonstrate how Mahaprajna and the samanis construct preksha dhyana as a form of modern yoga by appropriating scientific discourse and attributing physiological function to the yogic subtle body. I argue that preksha dhyana can be located at an intersection with late capitalist cultural processes as well as New Age spirituality insofar as its proponents participate in the transnational yoga market. Finally, I conclude with some thoughts on the successes and failures of the Terapanth in its attempt to globally disseminate preksha dhyana.

<p>In the present study, we examined the predictions of an attentional-associative model (Schmajuk, Lam, & Gray Journal of Experimental Psychology: Animal Behavior Processes, 22, 321-349, 1996) regarding the effect of attentional manipulations on both discrete and contextual conditioned inhibitors.</p><p>The SLG model assumes that non-reinforced presentations of an inhibitory conditioned stimulus (CS) do not decrease its inhibitory associations. However, the model predicts that extended presentations will decrease attention to the inhibitor, thereby, decreasing both the expression of its inhibitory power in a summation test and the rate of acquisition in a retardation test. The model also predicts that subsequent presentations of the inhibitory CS with a novel CS will increase both its inhibitory power in a summation test and the rate of acquisition in a retardation test. Using a predictive learning design in humans, Experiment 1 examined the predictions involving the summation tests, whereas Experiments 2 and 3 examined the predictions involving the retardation tests. Experimental results were in agreement with the predictions of the model. </p><p>The SLG model also predicts that a salient extinction context (CX) becomes inhibitory and prevents extinction of the excitatory CS-unconditioned stimulus (US) association. Although some data seem to contradict that prediction (e.g., Bouton and King, 1983, Bouton and Swartzentruber, 1986, 1989), Larrauri and Schmajuk (2008) indicated that the CX might not appear inhibitory in a summation test because attention to the CX decreases with many but not few extinction trials. In a human predictive learning experiment, we confirmed the model's predictions that the inhibitory power of the extinction CX can be detected after a few extinction trials when attention to the CX is still high, but not after many extinction trials once attention to the CX has decreased (Experiment 4), and even after many extinction trials by presenting novel CSs to increase attention to the unattended CX (Experiment 5). Furthermore, using an eye-tracker, we confirmed the model's explanation of Experiment 4 results by showing decreased overt attention to the CX after many but not after few extinction trials (Experiment 6).</p><p> Importantly, the view that the extinction CX becomes inhibitory allows the model to explain spontaneous recovery (because attention to the excitatory CS increases before attention to the inhibitory CX), renewal (because the inhibition provided by the extinction CX disappears), and reinstatement (the inhibitory CX becomes neutral or excitatory), as well as a very large number of other experimental results related to extinction. Based on the prediction of the SLG, model the implications of our results for the treatments of anxiety disorders were discussed.</p> / Dissertation

A growing body of scientific literature suggests that when individuals are asked to write about personally upsetting experiences, significant improvements in physical health are found. However, some attempts to replicate these findings and establish causal relationships between disclosure and health have yielded inconsistent results. Thus, in an effort to implement a narrative therapy utilizing a less typical sample, Pennebaker's self-guided writing therapy was utilized as an intervention for incarcerated women who had experienced traumatic events. Volunteer participants were randomly assigned to either the traumatic (experimental) or trivial topic (control) writing group, and were asked to write on these topics daily for four days. Objective medical utilization data was collected for the 12 weeks pre-intervention through 12 weeks post-intervention, and was supplemented by participant self-report measures. Institutional misconduct data was also collected for this period. No decreases in medical utilization or institutional misconduct were found. However, a significant increase in mental health utilization was demonstrated by the treatment group following the intervention. Implications of these findings and suggestions for future research in this area are discussed.

Schizophrenia is a complex disease that affects up to 1% of the general population. It is manifested by a variable number of negative, positive and disorganisation symptoms giving rise to an important diversity in the expression of this syndrome. The treatment of schizophrenia is mainly based on neuroleptic drugs that alleviate, to a variable extent, psychotic symptoms in the majority but not all the patients. Although its aetiology is still unknown, it is now well established that schizophrenia is a brain disease resulting from the combination of environmental and genetic risk factors. In spite of intensive research, no specific genes were convincingly associated with schizophrenia possibly because of the presence of genetic heterogeneity. In this work, it was hypothesised that schizophrenic patients with excellent long-term response (R) and those with very poor long-term response to conventional neuroleptics (NR) may differ, at least partially, with respect to the pathogenesis of their disease. In this thesis we aimed at validating this classification scheme and illustrating its usefulness for genetic studies. In accordance with this hypothesis, it was found that NR differ from R patients with respect to age at onset, premorbid social adjustment, neuropsychological profiles and family history of psychiatric disorders. Molecular genetic investigations identified 2 genes, the hGT1 and 5-HT2a-receptor genes, that were associated respectively with responsive and nonresponsive schizophrenia, thus showing the utility of categorising patients according to their therapeutic response. A third gene, called hSWI2/SNF2 was also found to be associated with schizophrenia irrespective of therapeutic response to neuroleptics. In addition, a potentially abnormal protein was detected in two schizophrenic patients but not in controls. In conclusion, the distinction of schizophrenic patients belonging to the two extremes of long-term responsiveness to neuroleptics may help in iden

Certains gènes, modulant la sérotonine (5-hydroxytryptamine, 5-HT), ont été associés aux tempéraments liés à l'anxiété. Une limitation dans la plupart de ces études est que les études sont de nature transversale et l'anxiété a été évaluée à un seul point dans le temps. De plus, seules quelques études ont été réalisées chez les enfants. Le but de la présente étude était d'étudier le rôle des gènes HTR2A et TPH2 dans le développement des trajectoires d’anxiété durant l’enfance. Les associations entre ces gènes, ces trajectoires, le diagnostic d’anxiété à l'âge adulte et les différences entre les sexes ont été examinées dans l'Étude Longitudinale des Enfants de Maternelle au Québec, composée de 3185 enfants recrutés en 1986-1987. Leur anxiété a été cotée par leur professeur annuellement entre 6 et 12 ans. Ces cotes ont été modélisées en trajectoires comportementales. Les données genotypées de 5-HT, disponibles pour 1068 personnes, ont été analysées en utilisant les statistiques du Chi-carré, des régressions logistiques et des analyses de variance. Sur les 37 polymorphismes étudiés, plusieurs ont été associés à la trajectoire de forte anxiété, tels le 5-HTR2A (rs1328684, rs95534511, rs1745837, rs7984966, 7330636) et TPH2 (rs11179050, rs11179052, rs1386498). Bien que les trajectoires d’anxiété en enfance n’aient pas prédit le diagnostic d'anxiété à 21 ans, les relations ont été trouvées entre ce diagnostic, HTR2A et les polymorphismes du nucléotide simple (PNS) de TPH2. On remarque que les PNS associés à l’anxiété durant l’enfance et l’âge adulte ne sont pas les mêmes. La force d'association entre les gènes étudiés et l'anxiété diffère entre les garçons et les filles. Cette étude est la première à identifier une association entre les variantes TPH2, 5-HTR2A et les trajectoires d’anxiété en enfance. Les études futures devraient reproduire les résultats dans d'autres échantillons, enquêter sur l'interaction avec les facteurs de stress, et étudier la pertinence fonctionnelle de la PNS. / A number of genes known to modulate serotonin (5-hydroxytryptamine, 5-HT) have been associated with anxiety-related temperaments. A limitation in most of these studies is that the studies are cross-sectional and anxiety has been measured at a single point in time. Furthermore, only a few studies have been done in children. The aim of the present study was to investigate the role of the HTR2A and TPH2 gene in the development of trajectories of anxiety in childhood/ adolescence. Associations between these genes, anxiety trajectories in childhood and anxiety diagnoses in adulthood were also investigated. Finally, gender differences were explored. Research questions were investigated in the Quebec Longitudinal Study of Kindergarten Children, consisting of 3185 boys and girls, selected in 1986-1987. Children`s anxiety was rated by their teacher every year between the age of 6 and 12 years. The ratings were modeled into behavioral trajectories. 5-HT genotyping data were available for 1068 cohort members. Data were analyzed using Chi-square statistics, logistic regressions and ANOVAs. Out of 37 investigated polymorphisms, several polymorphisms, such as 5-HTR2A (rs1328684, rs95534511, rs1745837, rs7984966, 7330636) and TPH2 (rs11179050, rs11179052, rs1386498) were associated with a high anxiety trajectory. Though trajectories of high anxiety in childhood did not predict an anxiety diagnosis at age 21, relationships were found between HTR2A and TPH2 SNPs and anxiety diagnosis at age 21. We note that the SNPs associated with anxiety were different between adults and children. The strength of association between the investigated genes and anxiety differed between boys and girls. This is the first study reporting an association with some HTR2A and TPH2 variants and trajectories of anxiety in children. Future studies should replicate the findings in other samples, investigate the interaction with stressors, and study the functional relevance of the SNPs

Plusieurs études antérieures ont proposé que la ménarche pouvait représenter une vulnérabilité accrue au développement de la dépression en augmentant la réactivité au stress chez les filles ayant atteint leur cycle menstruel. Dans la présente étude, les symptômes dépressifs et les niveaux de cortisol salivaire ont été mesurés chez 198 garçons et 142 filles (11 - 13 ans), et ce, à quatre reprises au cours de leur première année de transition vers l’école secondaire, une période de stress chez les adolescents. Les résultats ont montré que les filles qui avaient atteint la ménarche au moment de la transition vers le secondaire avait des niveaux significativement plus élevés de symptômes dépressifs et de cortisol salivaire entre l’automne et le printemps, comparativement aux filles qui n'avaient pas encore atteint la ménarche. Ces dernières présentaient des niveaux plus élevés de symptômes dépressifs que les filles sans et les garçons. Les filles sans ménarche présentaient d’avantages des niveaux de symptômes dépressives plus élevés que les garçons. En utilisant l’âge de ménarche comme variable catégorique, les résultats démontrent que les filles ayant eu leur ménarche plus jeunes présentent des symptômes dépressifs plus élevés tout au long de l'année scolaire, alors que les filles qui ont commencé leur cycle menstruel à l’âge dit ‘normal’ présentent des symptômes dépressifs transitoires. Globalement, ces résultats suggèrent que la ménarche est un indice significatif d’une vulnérabilité accrue pour les symptômes dépressifs et les niveaux de cortisol plus élevés chez les adolescentes qui font leur entrée au secondaire. Également, ces résultats suggèrent qu’un âge précoce de ménarche peut exposer à long-terme le cerveau en développement à des niveaux élévés de cortisol, rendant ainsi ce groupe d’adolescentes plus vulnérables à la dépression. / It has been proposed that the onset and/or earlier age at menarche confer greater vulnerability to depressive symptoms by increasing the reactivity of menarcheal girls to stressors associated with adolescence. In the present study, we measured depressive symptoms and salivary cortisol levels in 198 boys and 142 girls (11 -13 years) tested four times during their first year of transition into high school, a period known to be associated with stress among adolescents. Results showed that girls who had reached menarche before the transition to high school transit presented significantly higher depressive symptoms and salivary cortisol levels across the school year, when compared to girls who had not reached menarche and boys. Girls who had reached menarche presented significantly higher depressive scores than girls who had not reached menarche and boys. Girls who did had not reached menarche also scored significantly higher on depressive symptoms when compared to boys. When we divided the menarcheal girls as a function of age of onset, we found that girls with early age at menarche presented consistently higher scores for depressive symptoms from the start of the school year to early spring. Girls with on-time menarche scored higher for symptoms of depression, but these were more transitory. Altogether, these results show that onset of menarche is associated with greater depressive symptoms and higher cortisol levels in adolescent girls going through the stress of high school transition. These findings also suggest that early menarche may confer greater vulnerability to depression due to long-term exposure of the developing brain to high cortisol levels.