A obesidade tornou-se um dos mais graves problemas de saúde pública em todo o mundo, e o aumento na ingestão de alimentos hipercalóricos tem contribuído significativamente para o desenvolvimento desta doença. Este distúrbio metabólico pode ocasionar diversas outras comorbidades. Por outro lado, o estresse crônico, seja associado à obesidade ou não, leva a diferentes alterações neuroendócrinas e psicológicas. Estruturas cerebrais, especialmente o hipotálamo, estão envolvidas no controle do apetite. Atualmente, o hipocampo também tem sido associado ao controle do consumo alimentar. Neste contexto, o fator neurotrófico derivado do cérebro (BDNF) que é amplamente expresso em todas as regiões do cérebro e desempenha um papel importante na sobrevivência neuronal e na neuroplasticidade tem sido associado à regulação da homeostase energética e da ingestão alimentar. Assim, o objetivo desta tese foi investigar os efeitos da obesidade induzida por dieta hipercalórica sobre parâmetros neuroquímicos e comportamentais com base em dois protocolos experimentais. No primeiro protocolo experimental, 30 ratos Wistar adultos foram divididos igualmente em 2 grupos de acordo com modelo de dieta: grupo controle, que recebeu ração padrão, e grupo dieta de cafeteria, alimentado com dieta de cafeteria. O objetivo do protocolo experimental foi investigar os efeitos da obesidade induzida por dieta hipercalórica em parâmetros neuroquímicos e comportamentais. Foram avaliados ganho de peso, comportamento hiperfágico, comportamento do tipo ansioso e atividade locomotora no labirinto em cruz elevado e no aparato de campo aberto, respectivamente. Também foram avaliados os níveis de BDNF e a susceptibilidade ao dano induzido por H2O2 com liberação de lactato desidrogenase (LDH) em tecido hipocampal. Foi possível observar que a exposição à dieta de cafetaria durante 6 semanas resultou em obesidade, hiperfagia e aumento na atividade locomotora. Animais obesos mostraram diminuição dos níveis de BDNF e aumento da susceptibilidade a danos celulares no hipocampo. As alterações comportamentais em resposta à exposição à dieta de cafeteria podem ser relacionadas com os seus efeitos neuroquímicos no cérebro, e a deficiência na regulação do apetite (hiperfagia) que pode estar associada à perda de integridade do hipocampo. No segundo protocolo experimental, 32 ratos Wistar adultos foram divididos igualmente em 4 grupos de acordo com a dieta hipercalórica (modelo de dieta de cafeteria) e modelo de estresse crônico por restrição: grupo controle que recebeu dieta padrão; grupo estresse que foi exposto ao modelo de estresse crônico por restrição; grupo dieta hipercalórica, que recebeu a dieta hipercalórica e grupo estresse + dieta hipercalórica, que foi exposto ao modelo de estresse crônico por restrição e recebeu dieta hipercalórica. O objetivo foi avaliar o efeito da obesidade associada com o estresse crônico sobre os níveis centrais de BDNF. O peso do animal e a ingestão calórica foram empregados como parâmetros de obesidade enquanto o peso relativo da glândula adrenal foi empregado como parâmetro de estresse. Demonstrou-se que o estresse crônico por restrição, por 12 semanas, aumenta o peso da glândula adrenal, diminui os níveis de BDNF no hipocampo e está associado com decréscimo na ingestão de sacarose, caracterizando anedonia. O aumento na glândula adrenal demonstra a intensa estimulação desta estrutura. A diminuição no consumo de sacarose associada à diminuição do BDNF hipocampal pode sugerir um comportamento depressivo. Por outro lado, os ratos que receberam a dieta hipercalórica tiveram aumento na ingestão de calorias e tornaram-se obesos, resultado que foi associado a uma diminuição dos níveis de BDNF hipotálamo. / Obesity has become one of the most serious worldwide public health problems and increment on hypercaloric food intake has contributed significantly to the development this disease. This metabolic disorder can lead to various other comorbidities. On other hand chronic stress, whether associated with obesity or not, leads to different neuroendocrine and psychological changes. Brain structures, especially hypothalamus, are involved in food control. Currently the hippocampus also has been associated with energy intake. In this context, brain-derived neurotrophic factor (BDNF) that is widely expressed in all brain regions and plays an important role in neural survival and neuroplasticity has been implicated in the regulation of energy homeostasis and food intake. Thus, the aim of this thesis was to investigate the effects of hypercaloric diet-induced obesity associated or not to chronic stress by restriction on neurochemical and behavioral parameters based on two experimental protocols. In first experimental protocol 30 Wistar adults rats were equally divided on two groups according to diet model: control group that received standard rat chow and cafeteria diet group that received cafeteria diet model. The aim of the experiment protocol was to investigate the effects of hypercaloric diet-induced obesity on neurochemical and behavioral parameters. Were evaluated the weight gain, hiperfagic behavior, and the anxiety-like behavior and locomotor activity on Plus Maze and the Open Field tests, respectively. Were evaluated also the BDNF levels and susceptibility to H2O2-induced oxidative damage with LDH release of hippocampal tissue. In this experimental protocol was possible to observe that exposure to the cafeteria diet for six weeks resulted in obesity, hyperphagia and increased on locomotor activity. Obese animals showed decreased BDNF levels and increased susceptibility to cellular damage in the hippocampus. The behavioral consequences of exposure to the cafeteria diet may be related to its biochemical effects on the brain and impairments food intake regulation (hyperphagia) might be associated to the loss of hippocampal integrity. In second experimental protocol 32 Wistar adults rats were divided on four groups according to hypercaloric diet (cafeteria diet model) and chronic restraint stress model: (C) control total group that received standard rat chow; (S) stress group that was exposure to chronic restraint stress model and received standard rat chow; (HD) group that received hypercaloric diet and (SHD) stress group that was exposure to chronic restraint stress model and received hypercaloric diet. The aims of experimental protocol were to evaluate the effect of obesity associated with chronic stress on the BDNF central levels of rats. Obesity was controlled by analyzing the animals’ caloric intake and changes in body weight. As a stress parameter, was analyzed the relative adrenal gland weight. This experimental protocol demonstrated that chronic restraint stress for 12 weeks increased the weight of the adrenal gland, decrease BDNF levels in the hippocampus and is associated with a decrease in sucrose intake, characterized anhedonia. The increase in the adrenal gland demonstrates the intense stimulation of this structure. The decrease in the consumption of sucrose associated with decreased hippocampal BDNF may suggest a depressive behavior. On the other hand, mice that received hypercaloric diet had an increased caloric intake and became obese, which was associated with a decrease in BDNF levels hypothalamus.

O gás monóxido de carbono (CO) possui diversas funções no sistema nervoso central (SNC) funcionando como neuromodulador, como por exemplo da regulação da temperatura corporal, da nocicepção e mais recentemente, do comportamento emocional. Este neuromodulador gasoso é produzido pela ação da enzima heme oxigenase (HO), a qual é encontrada em diferentes áreas do SNC. Com destaque, esta enzima tem alta expressão no locus coeruleus (LC), o que sugere o envolvimento do CO na modulação de funções desempenhadas por esta estrutura. O LC localiza-se na ponte, sendo a maior origem da inervação noradrenérgica do SNC. Esta estrutura tem participação ativa na modulação das respostas relacionadas ao estresse, em particular, na modulação do comportamento emocional, desde que integra o Sistema de Inibição Comportamental (SIC), o qual inclui ainda o sistema septo-hipocampal e os núcleos da rafe. O SIC é responsável por comandar respostas defensivas de avaliação de risco, alerta e atenção, as quais podem ser eliciadas pela ansiedade. Dentro desta perspectiva, o presente estudo teve como objetivo avaliar se a ativação sistêmica da via HO-CO pode modular o comportamento emocional de ratos, e se há participação do LC. Assim, este trabalho avaliou se o tratamento sistêmico via intraperitoneal (i.p.) agudo (3 h antes) ou crônico (10 dias/2 vezes ao dia) com um liberador de monóxido de carbono (CORM-2), ou com indutor da enzima HO (CoPP), altera as respostas comportamentais no teste do labirinto em cruz elevado (LCE) e no teste claro-escuro (TCE) em ratos, bem como a expressão da enzima HO no LC. Em uma segunda etapa foi avaliado se a administração aguda de CORM-2 ou CoPP altera o comportamento avaliado no LCE e no TCE de ratos submetidos ao estresse crônico variado (ECV) por 10 dias. Os resultados mostraram que o CO induzido pela administração aguda ou crônica de CORM-2 ou CoPP possui efeito ansiolítico. Ainda, o tratamento com CORM-2 ou CoPP aumentou a expressão da enzima HO-1 em células localizadas no LC, sem alterar a imunorreatividade à enzima HO-2. Considerando os grupos submetidos ao estresse ECV, nem a ativação da via HO-CO ou o ECV apresentaram efeitos significativos nos comportamentos avaliados nos testes LCE e TCE. Os resultados do presente estudo sugerem que o tratamento sistêmico com drogas que modulam a liberação de CO possui claro efeito ansiolítico. Assim, é possível que o CO possa ser uma droga com potencial terapêutico para o tratamento de desordens neuropsiquiátricas. / The carbon monoxide gas (CO) has several functions in the central nervous system acting as a neuromodulator, such as in the body temperature regulation, nociception and more recently, in the emotional behavior modulation. This gas is produced by the action of the heme oxigenase enzyme (HO), which is found in different areas of the central nervous system (CNS). It is important to note that this enzyme has high expression in the locus coeruleus (LC), suggesting the involvement of CO in the modulation functions performed by this midbrain structure. LC is located in the pons, being the source of majority of the noradrenergic innervation of the CNS. This structure is intimately involved in the stress modulation responses, particularly in the emotional behavior regulation, since it integrates the Behavioral Inhibition System (BIS), which also includes septum-hippocampal system and raphe nucleus. The BIS is responsible for defensive responses like the risk assessment and alertness trigged by anxiety. Within this perspective, the present study was designed to evaluate whether the systemic HO-CO pathway can modulate emotional behavior of rats, and if the HO enzyme of the neurons located into LC is involved in this response. Thus, this study evaluated whether the acute systemic i.p. treatment (3 hours before) or chronic (10 days / 2 times a day) with a carbon monoxide releaser (CORM-2) or inducer of heme enzyme oxygenase (CoPP), is able to alter the behavioral responses in the elevated plus maze (EPM) and in the light-dark box test (LDB) in rats, and the HO enzyme expression in the LC. Furthermore, the effect of the acute administration of CORM-2 or CoPP was evaluated in the emotional behavior assessed in the EPM and LDB by rats submitted to unpredictable chronic stress (during 10 days). The results showed that the CO induced by acute or chronic administration of CORM-2 or CoPP has an anxiolytic-like effect. Furthermore, treatment with CORM-2 or CoPP promoted an increase of HO-1 enzyme expression in cells located in the LC without altering the immunoreactivity of HO-2 enzyme. Still, considering the rats subjected to stress UCS neither the activation of HO-CO pathway nor the UCS protocol altered the emotional behavior evaluated in the EPM and LDB tests. The results of this study suggest that systemic treatment with drugs that modulate the CO release has anxiolytic effect. Thus, it is possible that CO can be a potential drug therapeutic target for neuropsychiatric disorders.

Background Demands placed on individuals in occupational and social settings, as well as imbalances in personal traits and resources, can lead to chronic stress. The Trier Inventory for Chronic Stress (TICS) measures chronic stress while incorporating domain-specific aspects, and has been found to be a highly reliable and valid research tool. The aims of the present study were to confirm the German version TICS factorial structure in an English translation of the instrument (TICS-E) and to report its psychometric properties. Methods A random route sample of healthy participants (N = 483) aged 18–30 years completed the TICS-E. The robust maximum likelihood estimation with a mean-adjusted chi-square test statistic was applied due to the sample’s significant deviation from the multivariate normal distribution. Goodness of fit, absolute model fit, and relative model fit were assessed by means of the root mean square error of approximation (RMSEA), the Comparative Fit Index (CFI) and the Tucker Lewis Index (TLI). Results Reliability estimates (Cronbach’s α and adjusted split-half reliability) ranged from .84 to .92. Item-scale correlations ranged from .50 to .85. Measures of fit showed values of .052 for RMSEA (Cl = 0.50–.054) and .067 for SRMR for absolute model fit, and values of .846 (TLI) and .855 (CFI) for relative model-fit. Factor loadings ranged from .55 to .91. Conclusion The psychometric properties and factor structure of the TICS-E are comparable to the German version of the TICS. The instrument therefore meets quality standards for an adequate measurement of chronic stress.

A obesidade tornou-se um dos mais graves problemas de saúde pública em todo o mundo, e o aumento na ingestão de alimentos hipercalóricos tem contribuído significativamente para o desenvolvimento desta doença. Este distúrbio metabólico pode ocasionar diversas outras comorbidades. Por outro lado, o estresse crônico, seja associado à obesidade ou não, leva a diferentes alterações neuroendócrinas e psicológicas. Estruturas cerebrais, especialmente o hipotálamo, estão envolvidas no controle do apetite. Atualmente, o hipocampo também tem sido associado ao controle do consumo alimentar. Neste contexto, o fator neurotrófico derivado do cérebro (BDNF) que é amplamente expresso em todas as regiões do cérebro e desempenha um papel importante na sobrevivência neuronal e na neuroplasticidade tem sido associado à regulação da homeostase energética e da ingestão alimentar. Assim, o objetivo desta tese foi investigar os efeitos da obesidade induzida por dieta hipercalórica sobre parâmetros neuroquímicos e comportamentais com base em dois protocolos experimentais. No primeiro protocolo experimental, 30 ratos Wistar adultos foram divididos igualmente em 2 grupos de acordo com modelo de dieta: grupo controle, que recebeu ração padrão, e grupo dieta de cafeteria, alimentado com dieta de cafeteria. O objetivo do protocolo experimental foi investigar os efeitos da obesidade induzida por dieta hipercalórica em parâmetros neuroquímicos e comportamentais. Foram avaliados ganho de peso, comportamento hiperfágico, comportamento do tipo ansioso e atividade locomotora no labirinto em cruz elevado e no aparato de campo aberto, respectivamente. Também foram avaliados os níveis de BDNF e a susceptibilidade ao dano induzido por H2O2 com liberação de lactato desidrogenase (LDH) em tecido hipocampal. Foi possível observar que a exposição à dieta de cafetaria durante 6 semanas resultou em obesidade, hiperfagia e aumento na atividade locomotora. Animais obesos mostraram diminuição dos níveis de BDNF e aumento da susceptibilidade a danos celulares no hipocampo. As alterações comportamentais em resposta à exposição à dieta de cafeteria podem ser relacionadas com os seus efeitos neuroquímicos no cérebro, e a deficiência na regulação do apetite (hiperfagia) que pode estar associada à perda de integridade do hipocampo. No segundo protocolo experimental, 32 ratos Wistar adultos foram divididos igualmente em 4 grupos de acordo com a dieta hipercalórica (modelo de dieta de cafeteria) e modelo de estresse crônico por restrição: grupo controle que recebeu dieta padrão; grupo estresse que foi exposto ao modelo de estresse crônico por restrição; grupo dieta hipercalórica, que recebeu a dieta hipercalórica e grupo estresse + dieta hipercalórica, que foi exposto ao modelo de estresse crônico por restrição e recebeu dieta hipercalórica. O objetivo foi avaliar o efeito da obesidade associada com o estresse crônico sobre os níveis centrais de BDNF. O peso do animal e a ingestão calórica foram empregados como parâmetros de obesidade enquanto o peso relativo da glândula adrenal foi empregado como parâmetro de estresse. Demonstrou-se que o estresse crônico por restrição, por 12 semanas, aumenta o peso da glândula adrenal, diminui os níveis de BDNF no hipocampo e está associado com decréscimo na ingestão de sacarose, caracterizando anedonia. O aumento na glândula adrenal demonstra a intensa estimulação desta estrutura. A diminuição no consumo de sacarose associada à diminuição do BDNF hipocampal pode sugerir um comportamento depressivo. Por outro lado, os ratos que receberam a dieta hipercalórica tiveram aumento na ingestão de calorias e tornaram-se obesos, resultado que foi associado a uma diminuição dos níveis de BDNF hipotálamo. / Obesity has become one of the most serious worldwide public health problems and increment on hypercaloric food intake has contributed significantly to the development this disease. This metabolic disorder can lead to various other comorbidities. On other hand chronic stress, whether associated with obesity or not, leads to different neuroendocrine and psychological changes. Brain structures, especially hypothalamus, are involved in food control. Currently the hippocampus also has been associated with energy intake. In this context, brain-derived neurotrophic factor (BDNF) that is widely expressed in all brain regions and plays an important role in neural survival and neuroplasticity has been implicated in the regulation of energy homeostasis and food intake. Thus, the aim of this thesis was to investigate the effects of hypercaloric diet-induced obesity associated or not to chronic stress by restriction on neurochemical and behavioral parameters based on two experimental protocols. In first experimental protocol 30 Wistar adults rats were equally divided on two groups according to diet model: control group that received standard rat chow and cafeteria diet group that received cafeteria diet model. The aim of the experiment protocol was to investigate the effects of hypercaloric diet-induced obesity on neurochemical and behavioral parameters. Were evaluated the weight gain, hiperfagic behavior, and the anxiety-like behavior and locomotor activity on Plus Maze and the Open Field tests, respectively. Were evaluated also the BDNF levels and susceptibility to H2O2-induced oxidative damage with LDH release of hippocampal tissue. In this experimental protocol was possible to observe that exposure to the cafeteria diet for six weeks resulted in obesity, hyperphagia and increased on locomotor activity. Obese animals showed decreased BDNF levels and increased susceptibility to cellular damage in the hippocampus. The behavioral consequences of exposure to the cafeteria diet may be related to its biochemical effects on the brain and impairments food intake regulation (hyperphagia) might be associated to the loss of hippocampal integrity. In second experimental protocol 32 Wistar adults rats were divided on four groups according to hypercaloric diet (cafeteria diet model) and chronic restraint stress model: (C) control total group that received standard rat chow; (S) stress group that was exposure to chronic restraint stress model and received standard rat chow; (HD) group that received hypercaloric diet and (SHD) stress group that was exposure to chronic restraint stress model and received hypercaloric diet. The aims of experimental protocol were to evaluate the effect of obesity associated with chronic stress on the BDNF central levels of rats. Obesity was controlled by analyzing the animals’ caloric intake and changes in body weight. As a stress parameter, was analyzed the relative adrenal gland weight. This experimental protocol demonstrated that chronic restraint stress for 12 weeks increased the weight of the adrenal gland, decrease BDNF levels in the hippocampus and is associated with a decrease in sucrose intake, characterized anhedonia. The increase in the adrenal gland demonstrates the intense stimulation of this structure. The decrease in the consumption of sucrose associated with decreased hippocampal BDNF may suggest a depressive behavior. On the other hand, mice that received hypercaloric diet had an increased caloric intake and became obese, which was associated with a decrease in BDNF levels hypothalamus.

A obesidade tornou-se um dos mais graves problemas de saúde pública em todo o mundo, e o aumento na ingestão de alimentos hipercalóricos tem contribuído significativamente para o desenvolvimento desta doença. Este distúrbio metabólico pode ocasionar diversas outras comorbidades. Por outro lado, o estresse crônico, seja associado à obesidade ou não, leva a diferentes alterações neuroendócrinas e psicológicas. Estruturas cerebrais, especialmente o hipotálamo, estão envolvidas no controle do apetite. Atualmente, o hipocampo também tem sido associado ao controle do consumo alimentar. Neste contexto, o fator neurotrófico derivado do cérebro (BDNF) que é amplamente expresso em todas as regiões do cérebro e desempenha um papel importante na sobrevivência neuronal e na neuroplasticidade tem sido associado à regulação da homeostase energética e da ingestão alimentar. Assim, o objetivo desta tese foi investigar os efeitos da obesidade induzida por dieta hipercalórica sobre parâmetros neuroquímicos e comportamentais com base em dois protocolos experimentais. No primeiro protocolo experimental, 30 ratos Wistar adultos foram divididos igualmente em 2 grupos de acordo com modelo de dieta: grupo controle, que recebeu ração padrão, e grupo dieta de cafeteria, alimentado com dieta de cafeteria. O objetivo do protocolo experimental foi investigar os efeitos da obesidade induzida por dieta hipercalórica em parâmetros neuroquímicos e comportamentais. Foram avaliados ganho de peso, comportamento hiperfágico, comportamento do tipo ansioso e atividade locomotora no labirinto em cruz elevado e no aparato de campo aberto, respectivamente. Também foram avaliados os níveis de BDNF e a susceptibilidade ao dano induzido por H2O2 com liberação de lactato desidrogenase (LDH) em tecido hipocampal. Foi possível observar que a exposição à dieta de cafetaria durante 6 semanas resultou em obesidade, hiperfagia e aumento na atividade locomotora. Animais obesos mostraram diminuição dos níveis de BDNF e aumento da susceptibilidade a danos celulares no hipocampo. As alterações comportamentais em resposta à exposição à dieta de cafeteria podem ser relacionadas com os seus efeitos neuroquímicos no cérebro, e a deficiência na regulação do apetite (hiperfagia) que pode estar associada à perda de integridade do hipocampo. No segundo protocolo experimental, 32 ratos Wistar adultos foram divididos igualmente em 4 grupos de acordo com a dieta hipercalórica (modelo de dieta de cafeteria) e modelo de estresse crônico por restrição: grupo controle que recebeu dieta padrão; grupo estresse que foi exposto ao modelo de estresse crônico por restrição; grupo dieta hipercalórica, que recebeu a dieta hipercalórica e grupo estresse + dieta hipercalórica, que foi exposto ao modelo de estresse crônico por restrição e recebeu dieta hipercalórica. O objetivo foi avaliar o efeito da obesidade associada com o estresse crônico sobre os níveis centrais de BDNF. O peso do animal e a ingestão calórica foram empregados como parâmetros de obesidade enquanto o peso relativo da glândula adrenal foi empregado como parâmetro de estresse. Demonstrou-se que o estresse crônico por restrição, por 12 semanas, aumenta o peso da glândula adrenal, diminui os níveis de BDNF no hipocampo e está associado com decréscimo na ingestão de sacarose, caracterizando anedonia. O aumento na glândula adrenal demonstra a intensa estimulação desta estrutura. A diminuição no consumo de sacarose associada à diminuição do BDNF hipocampal pode sugerir um comportamento depressivo. Por outro lado, os ratos que receberam a dieta hipercalórica tiveram aumento na ingestão de calorias e tornaram-se obesos, resultado que foi associado a uma diminuição dos níveis de BDNF hipotálamo. / Obesity has become one of the most serious worldwide public health problems and increment on hypercaloric food intake has contributed significantly to the development this disease. This metabolic disorder can lead to various other comorbidities. On other hand chronic stress, whether associated with obesity or not, leads to different neuroendocrine and psychological changes. Brain structures, especially hypothalamus, are involved in food control. Currently the hippocampus also has been associated with energy intake. In this context, brain-derived neurotrophic factor (BDNF) that is widely expressed in all brain regions and plays an important role in neural survival and neuroplasticity has been implicated in the regulation of energy homeostasis and food intake. Thus, the aim of this thesis was to investigate the effects of hypercaloric diet-induced obesity associated or not to chronic stress by restriction on neurochemical and behavioral parameters based on two experimental protocols. In first experimental protocol 30 Wistar adults rats were equally divided on two groups according to diet model: control group that received standard rat chow and cafeteria diet group that received cafeteria diet model. The aim of the experiment protocol was to investigate the effects of hypercaloric diet-induced obesity on neurochemical and behavioral parameters. Were evaluated the weight gain, hiperfagic behavior, and the anxiety-like behavior and locomotor activity on Plus Maze and the Open Field tests, respectively. Were evaluated also the BDNF levels and susceptibility to H2O2-induced oxidative damage with LDH release of hippocampal tissue. In this experimental protocol was possible to observe that exposure to the cafeteria diet for six weeks resulted in obesity, hyperphagia and increased on locomotor activity. Obese animals showed decreased BDNF levels and increased susceptibility to cellular damage in the hippocampus. The behavioral consequences of exposure to the cafeteria diet may be related to its biochemical effects on the brain and impairments food intake regulation (hyperphagia) might be associated to the loss of hippocampal integrity. In second experimental protocol 32 Wistar adults rats were divided on four groups according to hypercaloric diet (cafeteria diet model) and chronic restraint stress model: (C) control total group that received standard rat chow; (S) stress group that was exposure to chronic restraint stress model and received standard rat chow; (HD) group that received hypercaloric diet and (SHD) stress group that was exposure to chronic restraint stress model and received hypercaloric diet. The aims of experimental protocol were to evaluate the effect of obesity associated with chronic stress on the BDNF central levels of rats. Obesity was controlled by analyzing the animals’ caloric intake and changes in body weight. As a stress parameter, was analyzed the relative adrenal gland weight. This experimental protocol demonstrated that chronic restraint stress for 12 weeks increased the weight of the adrenal gland, decrease BDNF levels in the hippocampus and is associated with a decrease in sucrose intake, characterized anhedonia. The increase in the adrenal gland demonstrates the intense stimulation of this structure. The decrease in the consumption of sucrose associated with decreased hippocampal BDNF may suggest a depressive behavior. On the other hand, mice that received hypercaloric diet had an increased caloric intake and became obese, which was associated with a decrease in BDNF levels hypothalamus.

O estresse crônico ou agudo pode alterar diversas funções relacionadas ao sistema cardiovascular, ocasionando doenças cardíacas. O sistema renina-angiotensina (SRA), importante participante do controle dessas funções, é profundamente afetado em resposta ao estresse. A angiotensina II (Ang II) é reconhecida como hormônio multifuncional que influencia diversos processos celulares importantes para a regulação da função vascular, incluindo regulação do tônus vascular, crescimento celular, dentre outros. Outro componente do SRA é a angiotensina 1-7 (Ang 1-7), suas ações vasculares envolvem aumento na produção de prostanóides vasodilatadores, óxido nítrico e fator hiperpolarizante derivado do endotélio. O objetivo do presente trabalho foi avaliar as conseqüências do estresse, agudo ou crônico, sobre as atividades vasomotoras da Ang II e da Ang 1-7, os mecanismos envolvidos na contração e relaxamento induzidos, respectivamente, por estes peptídeos e as modificações na expressão dos receptores AT1, AT2 e Mas, em carótida de ratos. O estresse crônico levou à diminuição do ganho de peso corpóreo dos animais, promoveu remodelamento das artérias carótidas, com significativo aumento da camada média acompanhada de redução da resposta de relaxamento da Ang 1-7, embora a expressão de seus receptores, do tipo Mas, estivesse aumentada. A maior expressão de receptores de Ang II, AT1 e AT2, desencadeada pelo estresse agudo não alterou a resposta contrátil deste peptídeo. Em carótidas de animais submetidos ao estresse crônico observa-se redução do Emax da Ang II e da Ang 1-7 após incubação com indometacina, sugerindo que prostanóides estão envolvidos na resposta vascular tanto da Ang II quanto da Ang 1-7 em situações de exposição prolongada ao estresse. A maior expressão de nitrotirosina em carótidas de animais expostos tanto ao estresse agudo quanto crônico, demonstra que o óxido nítrico e estresse oxidativo parecem estar relacionados às alterações vasomotoras, em resposta aos peptídeos Ang II e Ang 1-7. Foi evidenciado que o estresse agudo eleva significativamente os níveis plasmáticos de corticosterona e a produção de espécies reativas de oxigênio (EROs). Estes dados sugerem que os estresses agudo e crônico, por imobilização, alteram a expressão de receptores do SRA e a vasoatividade de carótidas em resposta à Ang II e Ang 1-7 em função de diferentes mecanismos celulares. / The chronic or acute stress can alter various functions of the cardiovascular system, causing heart disease. The renin-angiotensin system (RAS), a major participant in control of these functions, is profoundly affected in response to stress. Angiotensin II (Ang II) is recognized as a multifunctional hormone that influences many cellular processes important for the regulation of vascular function, including regulation of vascular tone, cell growth, among others. Another component of the RAS is angiotensin 1-7 (Ang 1-7), their actions involve an increase in vascular production of prostanoid vasodilators, nitric oxide and endothelium-derived hyperpolarizing factor. The aim of this study was to evaluate the consequences of chronic or acute stress on vasomotor activity of Ang II and Ang 1-7, the mechanisms involved in contraction and relaxation induced, respectively, by these peptides and the changes in the expression of AT1, AT2 and Mas in rat carotid artery. Chronic stress has led to decreased body weight gain of animals, promoted remodeling of carotid arteries with a significant increase in the medial layer accompanied by a reduction of the relaxation response to Ang 1-7, although the expression of their receptors (Mas) was increased. The highest expression of Ang II receptors, AT1 and AT2, triggered by acute stress did not alter the contractile response of this peptide. In carotid arteries of animals subjected to chronic stress is observed reduction of Emax of Ang II and Ang 1-7 after incubation with indomethacin, suggesting that prostanoids are involved in the vascular response of both Ang II and Ang 1-7 in exposed situations prolonged stress. The greater expression of nitrotyrosine in carotids from animals exposed to both acute or chronic stress, demonstrates that nitric oxide and oxidative stress appear to be related to vasomotor changes in response to peptides Ang II and Ang 1-7. It was shown that acute stress increases plasma levels of corticosterone and the production of reactive oxygen species (ROS). These data suggest that acute and chronic stress by immobilization, alter the expression of receptors of RAS and vasomotor activity in carotid artery in response to Ang II and Ang 1-7 by different cellular mechanisms.

Chronic stress can result in elevated circulating levels of glucocorticoid hormones in vertebrates, which can affect their stress response, their immune function, and eventually their fitness. I tested the effect of chronic corticosterone (CORT) elevation on the acute stress responsiveness, immune function, and body condition of free-living painted turtles (Chrysemys picta) in Gatineau Park, using slow-release exogenous CORT administration. While Silastic implants did not predictably elevate circulating CORT concentrations in painted turtles, injections of CORT-laden cocoa butter kept circulating levels elevated for up to 3 weeks, to concentrations likely physiologically and ecologically relevant for the species. I measured the acute CORT stress response, parasitaemia, heterophil-to-lymphocyte ratios, and total leukocyte counts after 1 week and 3 weeks, and determined body condition after 1 week, 3 weeks, and 1 year. Compared to sham and control turtles, I observed no effect of treatment on these hormonal, immune, and body condition metrics of stress, possibly because CORT mediates resource allocation only in the presence of additional immune or energy challenges, because of the masking effect of extrinsic factors, or because free, not total, CORT appears to be biologically active.

No description available.

Parents of children diagnosed with autism, a disease characterised with difficulty in speech, behaviour and language, experience chronic stress more than in any other developmental disorder. Outcomes of chronic stress in this regard are often associated with uncertain expectations of the future where current stressors are exuberated and future expectations are negated. Thinking about the future has been noted to contribute positive psychological functioning. Authors have, however, noted that some parents of autistic children are able to conceptualise positive future expectations in the mists of stressful current realities whilst using proactive coping strategies. Proactive coping literature has predominantly focused on situational characteristics and, to a lesser extent, on dispositional characteristics The relationship between dispositional characteristics - belief in just world, sense of coherence in relation to proactive coping is investigated in parents raising a child diagnosed with autism. Constructs were operationalised through the Orientation to Life Questionnaire (Antonovsky, 1987), Global Belief in Just World Scale (Lipkus, 1991), Reactions to Daily Life Questionnaire (Greenglass, 2002) and a demographic questionnaire. A cross-sectional correlational design consisting of a sample of 30 (n = 30) parents with children with autism was conducted. SPSS ver12 was used for analysis, which included both descriptive and inferential analysis. Inferential statistics included the Independent T-Test and analysis of variance (ANOVA) to analyse independence of the sample, and Spearman Rho correlations were used to test possible correlations between constructs. The small sample size precluded more advanced statistical manipulation of data. Open ended questions were analysed through a process of content analysis. The interpretation of results showed no significant differences between independent variables (e.g. age, gender, adjustment level of child) and constructs measured. Results of the correlational analysis indicated positive correlations between (i) belief in just world andproactive coping, (ii) sense of coherence and proactive coping as well as (iii) the sense of coherence (meaningfulness) subscale and proactive coping. No relationship was found between belief in just world and proactive coping. These results indicate that these dispositional characteristics can be associated with proactive coping and that belief in just world and sense of coherence who share similar theoretical underpinnings may have different predictor values. Qualitative results suggest that parents who engage in future oriented thinking and proactive coping strategies such as planning activities and social engagements often display higher levels of just world beliefs. The present study contributes to theoretical knowledge by providing insight into the relationships between constructs with regards to proactive coping in parents who experince chronic stress, by illustrating convergence and distinctiveness between constructs. Furthermore, knowledge was gained on the influence of dispositional characteristics on proactive coping strategies, seeing as how previous research primarily focused on situational characteristics. Practical applications of the results offer insight into coping processes of parents of children diagnosed with autism with specific reference to proactive coping which ultimately implicates the applicability value of future oriented therapeutic interventions for these families. Insight into the goals of parents and the daily challenges they face will furthermore assist the helping profession and support groups to provide effective support strategies. / Dissertation (MEd)--University of Pretoria, 2010. / Educational Psychology / unrestricted

L’adversité précoce présente une variété de conséquences nuisibles d’ordre cognitif, émotionnel, comportemental ou reliées à la santé. Plusieurs formes d’adversité durant l’enfance peuvent perturber le développement et générer du stress. L’adversité précoce est associée à de moindres volumes hippocampiques, ce qui pourrait être expliqué par l’effet neurotoxique de taux élevés de glucocorticoïdes générés par du stress chronique et l’influence d’expériences précoces et aversives. Les stratégies de navigation représentent la méthode selon laquelle un individu navigue dans l’environnement. En explorant un nouvel environnement, on peut choisir d’utiliser une stratégie spatiale dépendant de l’hippocampe basée sur une carte cognitive ou une stratégie réponse dépendant du noyau caudé basée sur une succession de virages. Nous voulions vérifier s’il existe une association entre les stratégies de navigation et l’adversité familiale précoce. Nous avons donc supposé que les individus utilisant une stratégie spatiale durant le Labyrinthe Virtuel 4/8 (une tâche de navigation à double solution) obtiendraient des scores d’adversité familiale précoce plus faibles que ceux employant une stratégie réponse. Nous supposions aussi que les enfants ayant des scores d’adversité familiale plus élevés présenteraient une performance de mémoire réduite comparativement à ceux aux scores plus faibles. Nous avons observé que les enfants avec un score élevé d’adversité familiale avaient une performance de mémoire réduite dans le Labyrinthe Virtuel 4/8 lorsque comparés au groupe à faible score. Cela soutient que la mémoire serait négativement affectée par l’adversité familiale vécue précocement. Cela suggère aussi l’existence potentielle d’une interaction plus complexe entre l’adversité précoce et les systèmes de mémoire. / Experiencing early adversity presents many varied detrimental consequences, whether they be cognitive, emotional, behavioral or health related. Various forms of adverse manifestations can perturb a child’s development and generate stress. Early adversity shows a lot of associations with lesser hippocampal volumes, which could be explained by the neurotoxic effect of elevated glucocorticoid levels due to chronic stress and the influence of adverse experience at an early age. Navigation strategies represent an individual’s method to navigate in an environment. When exploring a new environment, they may choose to use a hippocampus-dependent spatial strategy, which relies on a cognitive map, or a caudate nucleus-dependent response strategy based on a succession of turns. We wanted to verify if there was an association between navigation strategies and early family adversity. We hypothesised that individuals who use a spatial strategy on the 4/8 Virtual Maze (a dual-solution navigation task) would have a lesser cumulative score of early family adversity. It was also supposed that our group with a high risk of family adversity would manifest a reduced memory performance. We found that our group with a high risk of family adversity had shown reduced memory performance in the 4/8 Virtual Maze when compared to the low-risk group. This supported our initial supposition that memory would be affected by family adversity during early childhood. Our findings support the detrimental effect of early family adversity on memory performance. This also suggests the lingering of a more complex interaction between early adversity and the memory systems.