Stress affects virtually all organisms and can result in both physiological and behavioral changes. Conditioned defeat in Syrian hamsters is a model of stress-induced behavioral plasticity that occurs in a social context. In this model, hamsters are defeated by a larger, more aggressive counterpart. Defeated hamsters subsequently fail to defend their own territory and show striking and long-lasting increases in submissive behavior even when paired with a non-threatening counterpart. The present series of experiments seeks to identify the brain regions and molecular mediators that contribute to this behavioral plasticity. One brain region that has been overlooked by our laboratory is the hippocampus. The results of the first study suggested that the ventral, but not dorsal, hippocampus is important for the acquisition of conditioned defeat as temporary inactivation of the ventral hippocampus prior to defeat training significantly reduced submissive and defensive behaviors when hamsters were tested with a non-aggressive intruder. Next, we sought to identify a potential molecular mediator of social stress-induced behavioral plasticity in hamsters identified as winners or losers after a fight. Using in situ hybridization for brain-derived neurotrophic factor (BDNF) mRNA, we showed that winning and losing hamsters exhibited differences in BDNF mRNA in several regions including the basolateral and medial amygdala as well as the dentate gyrus of the dorsal hippocampus and CA1 of the ventral hippocampus. We next showed that neurotrophic activity in the basolateral amygdala is important for the acquisition of conditioned defeat because K252a infused into the basolateral amygdala prior to defeat training by an aggressive counterpart, significantly decreased submissive and defensive behavior during subsequent testing. Finally, existing data suggest that the amygdala and hippocampus interact to modulate the formation of emotional memories. To test the hypothesis that the basolateral amygdala and ventral hippocampus interact to mediate the behavioral plasticity observed in conditioned defeat, we simultaneously inactivated these regions either contralaterally or ipsilaterally prior to social defeat. Our results suggest that BLA and VHPC interact to mediate the acquisition of conditioned defeat, however, the nature of this interaction remains to be determined.

A growing body of evidence suggests that social stress contributes to the pathogenesis of neurodegenerative diseases, such as multiple sclerosis (MS). For example, prior research has shown that social disruption (SDR) stress behaviorally and immunologically exacerbates Theiler’s murine encephalomyelitis virus (TMEV) infection. TMEV infection results in acute infection of the central nervous system (CNS) followed by a chronic demyelinating autoimmune disease, similar to that seen in MS. Research suggests that social stress exerts these effects by altering the immune response to infection. More specifically, it is hypothesized that SDR sensitizes the acute inflammatory response to infection and suppresses T cell effector function in the acute phase of disease. It was demonstrated that SDR is sufficient to alter inflammation. Exposure to a single session of SDR increases IL-­‐1β mRNA expression; however, IL-­‐6 mRNA expression, but not IL-­‐1β, is up regulated in response to chronic SDR. Furthermore, chronic SDR prior to infection resulted in increased infection related central IL-­‐6 and IL-­‐1β mRNA expression, and central administration of IL-­‐6 neutralizing antibody during SDR reverses this increase in neuroinflammation. This suggests that SDR sensitizes infection related CNS inflammation through an up-­‐regulation of IL-­‐6. Chronic SDR prior to infection also resulted in enhanced CNS viral titers and suppression of virus-­‐induced CD4 and CD8 T cell IFN-­‐γ release within the CNS. As a whole, this research indicates that SDR exacerbates the disease course of TMEV infection by altering the central innate and adaptive immune response to infection. This research enhances our understanding of the mechanisms by which social stress exacerbates neurodegenerative disease pathogenesis.

Stress is known to alter immune function, both in positive and negative ways. The disparate effects of stress on immune function remains an active area of investigation. This thesis investigates how the application of social disruption stress either prior to or concurrent with infection alters the neuropathogenesis of Theiler's murine encephalitis virus. Experiment 1 verified that social disruption prior to infection exacerbated the course of infection. Experiment 2 examined application of social disruption concurrent with infection, and found that this may produce a delay in symptom onset, and possibly a protective effect. Experiment 3 directly compared the two schedules to each other. The previous findings were replicated and expanded with additional measures (both behavioral and physiological) that further verified the earlier findings. Social disruption applied prior to infection resulted in greater behavioral and physiological exacerbation of the disease. Concurrently applied stress remained protective or inhibitory in the disease progression. Timing of stress is one of several quantitative aspects of stress that has been found to impact the stress-immune interaction and should be further investigated.

Chronic major depressive disorder (CMDD) is a common and debilitating illness. Its pathophysiology needs further elucidation, before more effective targeted treatments can be developed for this condition. To gain a better understanding of the psychobiology of CMDD, three interconnected studies were conducted that examined the interplay between chronic depression, cortisol responses, and personality. Study 1 examined cortisol responses to the Trier Social Stress Test (TSST) in CMDD participants (n=29) as compared to healthy controls (n=28). It was hypothesized that cortisol responses would be greater in the CMDD population. Results indicated that females with CMDD had increased cortisol output compared to female controls, a pattern consistent with the hypothesis. However, males with CMDD had decreased cortisol responses compared to male controls. These results suggest that cortisol responses to social stress are altered in those with CMDD; however, females and males experience fundamentally different changes. Study 2 examined moderating effects of personality on cortisol responses to the TSST in those with CMDD (n=51) as compared to healthy controls (n=57). It was hypothesized that higher neuroticism and/or lower extraversion would be associated with increased cortisol responses in CMDD participants. As hypothesized, lower extraversion was associated with increased cortisol reactivity in those with CMDD but not in healthy controls. However, no association was found between neuroticism and cortisol responses. These findings could support the notion that lower extraversion is a vulnerability marker for chronic depression and thus a possible target for treatment. Study 3, evaluated the cortisol awakening response (CAR) in CMDD participants (n=27) compared to healthy controls (n=30). It was hypothesized that such awakening responses would be more pronounced in the depressed population compared to controls. Contrary to expectation, no differences were found between the groups. However, lower extraversion was associated with a lower CAR in both CMDD and healthy controls, a finding that was not anticipated a priori. These interconnected studies suggest that examining relationships between depression, cortisol responses, and personality, can assist with identifying distinct psychobiological profiles in those with chronic depression. It is proposed that this strategy will improve the likelihood of developing more targeted treatments for this population.

Chronic major depressive disorder (CMDD) is a common and debilitating illness. Its pathophysiology needs further elucidation, before more effective targeted treatments can be developed for this condition. To gain a better understanding of the psychobiology of CMDD, three interconnected studies were conducted that examined the interplay between chronic depression, cortisol responses, and personality. Study 1 examined cortisol responses to the Trier Social Stress Test (TSST) in CMDD participants (n=29) as compared to healthy controls (n=28). It was hypothesized that cortisol responses would be greater in the CMDD population. Results indicated that females with CMDD had increased cortisol output compared to female controls, a pattern consistent with the hypothesis. However, males with CMDD had decreased cortisol responses compared to male controls. These results suggest that cortisol responses to social stress are altered in those with CMDD; however, females and males experience fundamentally different changes. Study 2 examined moderating effects of personality on cortisol responses to the TSST in those with CMDD (n=51) as compared to healthy controls (n=57). It was hypothesized that higher neuroticism and/or lower extraversion would be associated with increased cortisol responses in CMDD participants. As hypothesized, lower extraversion was associated with increased cortisol reactivity in those with CMDD but not in healthy controls. However, no association was found between neuroticism and cortisol responses. These findings could support the notion that lower extraversion is a vulnerability marker for chronic depression and thus a possible target for treatment. Study 3, evaluated the cortisol awakening response (CAR) in CMDD participants (n=27) compared to healthy controls (n=30). It was hypothesized that such awakening responses would be more pronounced in the depressed population compared to controls. Contrary to expectation, no differences were found between the groups. However, lower extraversion was associated with a lower CAR in both CMDD and healthy controls, a finding that was not anticipated a priori. These interconnected studies suggest that examining relationships between depression, cortisol responses, and personality, can assist with identifying distinct psychobiological profiles in those with chronic depression. It is proposed that this strategy will improve the likelihood of developing more targeted treatments for this population.

Thesis (M.A. (Health Social Sciences))--Mahidol University, 2000.

Made available in DSpace on 2014-06-11T19:22:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-02-18Bitstream added on 2014-06-13T20:28:42Z : No. of bitstreams: 1 boscolo_cnp_me_jabo.pdf: 894828 bytes, checksum: 888a8e7f88c78fee4acfad75297e24e1 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Animais com a mesma habilidade de luta podem lutar por mais tempo e intensamente do que em confrontos assimétricos. Assim, a seleção de peixes pela similaridade de tamanho em manejos da piscicultura pode causar um aumento das interações agressivas e levar à instabilidade social em peixes socialmente organizados. Assim, testou-se a hipótese de que o agrupamento de animais de tamanhos semelhantes aumenta as interações agressivas entre machos de tilápia-do-nilo, linhagem GIFT. Este, por sua vez, aumenta o estresse social e desestabiliza a hierarquia social. Foram comparados dois tratamentos: um grupo homogêneo (HM), formado por cinco machos revertidos com variação de tamanho entre 9,0 e 9,4 cm; e um grupo heterogêneo (HT), formado por cinco animais de tamanhos variando entre 7,5 e 11,5 cm (n=16 para cada tratamento). Os peixes foram mantidos nesses grupos por seis dias, nos quais as interações agonísticas foram registradas a partir do segundo dia de agrupamento (10 min dia-1 – 5 sessões de observação). Níveis de cortisol plasmático e taxa de crescimento específico (TCE) foram utilizados para inferir estresse social. A frequência de interações agonísticas foi maior no HM (média ± S.E: HM = 302,06± 20,13 x 10 min-1; HT = 151,06 ± 13,35 x 10 min-1). Mudanças na posição social ocorreram neste grupo, indicando instabilidade social. Entretanto, os níveis de cortisol (HM = 27,54 ± 3,02 ng mL-1; HT = 24,42 ± 2,41 ng mL-1) e TCE (HM = -0,53 ± 0,04%; HT = -0,64 ± 0,08%) foram similares entre os tratamentos. Dessa forma, conclui-se que o agrupamento de peixes de tamanhos semelhantes aumenta as interações agressivas e desestabiliza a hierarquia social. Assim, apesar de não terem sido encontradas diferenças nos indicadores de estresse, pode-se concluir, com base em comportamento, que o agrupamento de animais de tamanhos semelhante reduz o bem-estar de peixes sociais... / Animals with similar fighting ability can fight intensely and longer than animals in 27 asymmetric contests. Thus, the selection of fish by size similarity in husbandry might increase 28 aggressive interactions, and lead to social instability in socially organized fish. We tested the 29 hypothesis that grouping similar size animals increases aggressive interactions between males of 30 Genetic Improved Farmed Tilapia (GIFT). This, in turn, enhances social stress and destabilizes 31 social hierarchy. We compared two treatments: a homogeneous group (HM) formed by five 32 males ranging in size from 9.0 to 9.4 cm, and a heterogeneous group (HT) formed by five males 33 sizing from 7.5 to 11.5 cm (n = 16 each treatment). The fish were kept in these groups for six 34 days, in which agonistic interactions were video-recorded daily from the second day of 35 grouping (10 min/ day – five observation sessions). Plasma cortisol levels and specific growth 36 rate (SGR) were used to infer stress level. The frequency of agonistic interactions was higher in 37 the HM (mean ± S.E.: HM = 302.06 ± 20.13 x 50 min-1; HT = 151.06 ± 13.35 x 50 min-1). 38 Changes in social position occurred over time in this group, indicating social instability. 39 However, cortisol levels (HM = 27.54 ± 3.02 ng.mL-1; HT = 24.42 ± 2.41 ng.mL-1) and SGR 40 (HM = -0.53 ± 0.04 %; HT = -0.64 ± 0.08 %) were similar between treatments. Thus, we 41 conclude that the grouping of similar size fish increases aggressive interactions and destabilizes 42 social hierarchy. Although no significant differences were found on indicators of stress we can 43 conclude, based on behavior, that groups of similar sized animals reduces the welfare in social 44 fish, because chances of injuries are higher than in heterogeneous groups

abstract: Psychological distress occurs at disproportionate rates among minority groups and individuals with lower socioeconomic status. This dissertation focuses on the relationship between living in a disadvantaged neighborhood and distress among Latinos, the formal and informal organizations that mediate the direct and indirect relationship between disadvantage and distress in this population, and the differences of social stress processes based on aspects of Latino social status, linguistic acculturation status, and the percentage of residents in the neighborhood that identify as Latino. This dissertation focuses its investigation on Latinos living in Chicago, specifically asking: In a metropolitan city, can the presence of formal and informal community organizations protect Latinos living in disadvantage neighborhoods from experiencing psychological distress? The findings demonstrate an indirect association between disadvantage and distress though objective disorganization and perception of disorganization. Both the density of community centers and block watch had an indirect protective effect, mediating the relationship between neighborhood disadvantage and distress, but did not decrease the indirect effect of disadvantage on distress through objective or perceptions of disorganization. The results of this dissertation suggest that changes to a neighborhood's environment may decrease population rates of distress in disadvantaged neighborhoods. / Dissertation/Thesis / Ph.D. Social Work 2014

No description available.

Hoarding disorder (HD) is characterized by (a) the acquisition of and inability to discard a large number of possessions; (b) clutter that interferes with the use of appliances and general living areas in the home; and (c) clinically significant distress or impairment in functioning. Although previous studies have reported that individuals with HD exhibit emotional dysregulation when discarding personal items, this investigation is the first to examine the biological indices of distress. The current study aimed to examine whether individuals with HD differed from healthy controls in their psychological and biological responses to a general psychosocial stressor and to investigate whether individual differences in stress response relate to differences in symptom severity and impairment. Twenty-one individuals with HD and 22 healthy controls (CTLs) completed the Trier Social Stress Task and self-reported affect and salivary cortisol responses to the stressor were assessed. Individuals with HD did not significantly differ compared to CTLs in their salivary cortisol levels in relation to the stressor. However, individuals with HD significant-ly differed compared to CTLs in their subjective levels of distress in relation to the stressor. Contrary to our hypotheses, responses to stress were not significantly correlated with measures of symptom severity and impairment due to hoarding. The current findings indicate that individuals with HD exhibit a greater self-reported emotional response to a general stressor. The implications of these findings are discussed. / Thesis / Master of Science (MS)