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1.
Article in English | WPRIM | ID: wpr-880327

ABSTRACT

BACKGROUND@#Prenatal stress can cause neurobiological and behavioral defects in offspring; environmental factors play a crucial role in regulating the development of brain and behavioral; this study was designed to test and verify whether an enriched environment can repair learning and memory impairment in offspring rats induced by prenatal stress and to explore its mechanism involving the expression of insulin-like growth factor-2 (IGF-2) and activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus of the offspring.@*METHODS@#Rats were selected to establish a chronic unpredictable mild stress (CUMS) model during pregnancy. Offspring were weaned on 21st day and housed under either standard or an enriched environment. The learning and memory ability were tested using Morris water maze and Y-maze. The expression of IGF-2 and Arc mRNA and protein were respectively measured by using RT-PCR and Western blotting.@*RESULTS@#There was an elevation in the plasma corticosterone level of rat model of maternal chronic stress during pregnancy. Maternal stress's offspring exposed to an enriched environment could decrease their plasma corticosterone level and improve their weight. The offspring of maternal stress during pregnancy exhibited abnormalities in Morris water maze and Y-maze, which were improved in an enriched environment. The expression of IGF-2, Arc mRNA, and protein in offspring of maternal stress during pregnancy was boosted and some relationships existed between these parameters after being exposed enriched environment.@*CONCLUSIONS@#The learning and memory impairment in offspring of prenatal stress can be rectified by the enriched environment, the mechanism of which is related to the decreasing plasma corticosterone and increasing hippocampal IGF-2 and Arc of offspring rats following maternal chronic stress during pregnancy.


Subject(s)
Animals , Cytoskeletal Proteins/metabolism , Female , Gene Expression Regulation , Hippocampus/metabolism , Insulin-Like Growth Factor II/metabolism , Learning , Learning Disabilities/psychology , Male , Memory Disorders/psychology , Nerve Tissue Proteins/metabolism , Pregnancy , Prenatal Exposure Delayed Effects/psychology , Random Allocation , Rats , Rats, Wistar , Social Environment , Stress, Psychological/genetics
2.
Rev. Assoc. Med. Bras. (1992) ; 65(6): 830-833, June 2019. graf
Article in English | LILACS | ID: biblio-1012983

ABSTRACT

SUMMARY OBJECTIVE Even though stress has been long known as a provocative factor for Graves' disease, its relationship with Hashimoto's thyroiditis is more controversial. Studies on this topic are scanty. This paper aims to report a case of stress-induced Hashitoxicosis. RESULTS Here we report a case of Hashitoxicosis induced by a psychological stressful event in a 28-year-old woman with Hashimoto's thyroiditis. She had remained stably euthyroid for 12 years. She was first observed in April 2016, while euthyroid. She came back after 11 months because of fatigue and palpitations, in the absence of neck pain. Thyroid function tests revealed moderate thyrotoxicosis (undetectable TSH; FT4 36.94 pmol/L, normal values 9.0-24.46; FT3 13.50 pmol/L, normal values 3.07-6.14) with negative TSH-receptor antibodies. In the previous three months, she had experienced a psychological stressful event. Inflammatory markers were negative, and the white cell count was normal. Thyroid ultrasound revealed a modest increase in vascularization. Transient subclinical hypothyroidism ensued after seven weeks and spontaneously recovered. On the last visit, the patient was still on euthyroidism. (TSH 1.01 mU/L; FT4 9.22 pmol/L; FT3 3.98 pmol/L). We also performed HLA serotyping and genotyping. CONCLUSION This case demonstrates that, similarly to Graves' disease, Hashitoxicosis can also be triggered by stressful life events.


RESUMO OBJETIVO Mesmo que o estresse seja conhecido há muito tempo como um fator provocativo para a doença de Graves, sua relação com a tireoidite de Hashimoto é mais controversa. Estudos sobre esse tema são escassos. O objetivo deste artigo é relatar um caso de Hashitoxicose induzida por estresse. RESULTADOS Aqui nós relatamos um caso de Hashitoxicose induzido por um evento psicológico estressante em uma mulher de 28 anos com tireoidite de Hashimoto. Ela permaneceu estável eutireoidiana por 12 anos. Ela veio a nossa observação pela primeira vez em abril de 2016, enquanto eutireoidiana. Voltou após 11 meses por causa de fadiga e palpitações, na ausência de dor no pescoço. Testes de função tireoidiana revelaram uma tireotoxicose moderada (TSH indetectável; T4F 36,94 pmol/L, valores normais 9,0-24,46; FT3 13,50 pmol/L, valores normais 3,07-6,14) com anticorpos negativos para o receptor de TSH. Nos últimos três meses ela experimentou um evento psicológico estressante. Os marcadores inflamatórios foram negativos e a contagem de leucócitos foi normal. A ultrassonografia da tireoide revelou um aumento modesto da vascularização. Hipotireoidismo subclínico transitório ocorreu após sete semanas e se recuperou espontaneamente. Na última visita, a paciente ainda estava em eutireoidismo. (TSH 1,01 mU/L; FT4 9,22 pmol/L; FT3 3,98 pmol/L). Também realizamos a sorotipagem e a genotipização do HLA. CONCLUSÃO Este caso demonstra que, similarmente à doença de Graves, também a Hashitoxicose pode ser desencadeada por eventos estressantes da vida.


Subject(s)
Humans , Female , Adolescent , Stress, Psychological/complications , Hashimoto Disease/psychology , HLA Antigens/genetics , Stress, Psychological/genetics , Thyroxine/blood , Thyrotropin/blood , Hashimoto Disease/genetics , Serogroup , Genotype
3.
Arq. bras. cardiol ; 112(1): 67-75, Jan. 2019. tab, graf
Article in English | LILACS | ID: biblio-973833

ABSTRACT

Abstract Background: Prenatal stress may increase risk of developing cardiovascular disorders in adulthood. The cardiotoxic effects of catecholamines are mediated via prolonged adrenergic receptor stimulation and increased oxidative stress upon their degradation by monoamine oxidase A (MAO-A). Objectives: We investigated long-term effects of prenatal stress on β (1, 2, 3) adrenergic receptors and MAO-A gene expression in the hearts of adult rat offspring. Methods: Pregnant rats were exposed to unpredictable mild stress during the third week of gestation. RNA was isolated from left ventricular apex and base of adult offspring. Quantitative PCR was used to measure gene expression in collected ventricular tissue samples. The level of significance was set to p < 0.05. Results: β3 adrenergic receptor mRNA was undetectable in rat left ventricle. β1 adrenergic receptor was the predominantly expressed subtype at the apical and basal left ventricular myocardium in the control females. Male offspring from unstressed mothers displayed higher apical cardiac β1 than β2 adrenergic receptor mRNA levels. However, β1 and β2 adrenergic receptor mRNAs were similarly expressed at the ventricular basal myocardium in males. Unlike males, prenatally stressed females exhibited decreased β1 adrenergic receptor mRNA expression at the apical myocardium. Prenatal stress did not affect cardiac MAO-A gene expression. Conclusions: Collectively, our results show that prenatal stress may have exerted region- and sex-specific β1 and β2 adrenergic receptor expression patterns within the left ventricle.


Resumo Fundamento: Estresse pré-natal pode aumentar os riscos de desenvolver doenças cardiovasculares na idade adulta. Os efeitos cardiotóxicos de catecolaminas são mediados pela estimulação prolongada dos receptores adrenérgicos e pelo aumento do estresse oxidativo após sua degradação pela monoamina oxidase A (MAO-A). Objetivos: Investigamos os efeitos a longo prazo de estresse pré-natal nos receptores β (1, 2, 3) adrenérgicos e na expressão do gene MAO-A nos corações da prole adulta de ratos. Método: Ratas prenhes foram expostas a estresse crônico moderado imprevisível durante a terceira semana de gestação. O RNA foi isolado do ápice e da base do ventrículo esquerdo da prole adulta. Utilizou-se PCR quantitativa em tempo real para medir a expressão gênica nas amostras de tecido ventricular coletadas. O nível de significância foi estabelecido em p < 0,05. Resultados: Foi indetectável o mRNA do receptor adrenérgico β3 no ventrículo esquerdo dos ratos. O receptor adrenérgico β1 foi o subtipo mais expresso no miocárdio ventricular esquerdo apical e basal nas fêmeas controle. A prole masculina das mães não estressadas apresentou níveis cardíacos apicais de mRNA do receptor adrenérgico β1 mais altos do que os de β2. Porém, mRNAs dos receptores adrenérgicos β1 e β2 foram expressos de forma semelhante no miocárdio basal ventricular na prole masculina em geral. Ao contrário da prole masculina, a prole feminina exposta ao estresse pré-natal exibiu uma expressão diminuída do mRNA do receptor adrenérgico β1 no miocárdio apical. O estresse pré-natal não afetou a expressão gênica de MAO-A cardíaca. Conclusões: Coletivamente, nossos resultados mostram que estresse pré-natal pode ter exercido padrões de expressão região- e sexo-específica dos receptores adrenérgicos β1 e β2 no ventrículo esquerdo.


Subject(s)
Animals , Female , Pregnancy , Prenatal Exposure Delayed Effects/metabolism , Stress, Psychological/metabolism , Pregnancy, Animal/psychology , Receptors, Adrenergic, beta/analysis , Monoamine Oxidase/analysis , Myocardium/metabolism , Prenatal Exposure Delayed Effects/psychology , Reference Values , Stress, Psychological/genetics , Time Factors , RNA, Messenger/analysis , Cardiovascular Diseases/etiology , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/psychology , Gene Expression , Sex Factors , Receptors, Adrenergic, beta/genetics , Rats, Wistar , Adrenocorticotropic Hormone/blood , Real-Time Polymerase Chain Reaction , Heart Ventricles/metabolism , Monoamine Oxidase/genetics , Mothers/psychology
4.
Psicol. reflex. crit ; 28(4): 829-839, out.-dez. 2015. graf
Article in Portuguese | LILACS, INDEXPSI | ID: lil-763108

ABSTRACT

Cuidados maternais são experiências do início da vida que têm sido consistentemente relacionados com alterações na expressão gênica por meio de mecanismos epigenéticos como a metilação do DNA ou a modificação de suas histonas. O objetivo deste trabalho é apresentar uma investigação teórica sobre cuidados maternais enquanto evento ambiental que pode produzir alterações epigenéticas atuantes na composição da vulnerabilidade ao estresse. A investigação teve por base estudos empíricos e de revisão de literatura com animais não humanos sobre Epigenética, estresse e cuidados maternais. Apresenta também alguns estudos com humanos que mostram tais efeitos, destacando-se aqueles que influenciam ou são influenciados pelo comportamento operante. A partir da investigação realizada encontrou-se que cuidados maternais pós-parto são uma condição ambiental que produz efeitos no eixo hipotálamo-pituitária-adrenal (HPA), participando da composição da vulnerabilidade ao estresse. Seus possíveis efeitos fisiológicos no condicionamento operante sinalizam alternativas para intervenções baseadas na plasticidade da formação do epigenoma. Este conhecimento, além de promover a aproximação entre a Epigenética e a Análise do Comportamento em nível básico por meio de estudos com animais não humanos, poderá contribuir em nível aplicado para um melhor entendimento do neurodesenvolvimento infantil e adequado planejamento de intervenções efetivas com mães e filhos. (AU)


Maternal care is an early life experience that has been consistently related to alterations in the genetic expression through epigenetic mechanisms such as DNA methylation or DNA histone modification. The present study aims to present a theoretical investigation about maternal care as an environmental event that may produce epigenetic alterations related to the biological bases of stress vulnerability. The research was based on empirical studies as well as literature review on non-human animals concerning epigenetics, stress and maternal care. It also presents some studies on humans that show such effects, particularly the ones that influence or are influenced by the operant behavior. Post-natal maternal care is found to cause effects on the hypothalamic-pituitary-adrenal (HPA) axis activity participating in the building of stress vulnerability. Its possible physiological effects on the operant conditioning point out to alternatives to intervention based on the plasticity of the epigenome formation. This knowledge enhances the proximity between Epigenetics and Behavior Analysis at a basic level through studies with non-human animals and at an applied level through a better understanding of child neurodevelopment and proper planning of effective intervention with mothers and children. (AU)


Subject(s)
Animals , Rats , Stress, Psychological/genetics , Child Care/psychology , Epigenomics , Mother-Child Relations/psychology , Postpartum Period , Neurodevelopmental Disorders
5.
Indian J Hum Genet ; 2012 Jan; 18(1): 20-33
Article in English | IMSEAR | ID: sea-139437

ABSTRACT

Depression is a term that has been used to describe a variety of ailments, ranging from minor to incapacitating. Clinically significant depression, termed as major depression, is a serious condition characterized not only by depressed mood but also by a cluster of somatic, cognitive, and motivational symptoms. Significant research efforts are aimed to understand the neurobiological as well as psychiatric disorders, and the evaluation of treatment of these disorders is still based solely on the assessment of symptoms. In order to identify the biological markers for depression, we have focused on gathering information on different factors responsible for depression including stress, genetic variations, neurotransmitters, and cytokines and chemokines previously suggested to be involved in the pathophysiology of depression. The present review illustrates the potential of biomarker profiling for psychiatric disorders, when conducted in large collections. The review highlighted the biomarker signatures for depression, warranting further investigation.


Subject(s)
Biomarkers/genetics , Chemokines , Cytokines , Depression/genetics , Depressive Disorder/genetics , Genetic Markers/genetics , Genetic Variation/genetics , Humans , Neurotransmitter Agents , Signs and Symptoms , Stress, Psychological/genetics
6.
Rev. bras. psiquiatr ; 29(supl.1): s13-s18, maio 2007. ilus
Article in Portuguese | LILACS | ID: lil-452227

ABSTRACT

OBJETIVO: Revisar os achados recentes sobre a relação entre estresse, eixo hipotálamo-pituitária-adrenal e depressão, na tentativa de explicar um endofenótipo de vulnerabilidade para o desenvolvimento da depressão. MÉTODO: Revisão não sistemática da literatura baseada na hipótese de endofenótipo. RESULTADOS: A depressão está relacionada à hipercortisolemia em muitos pacientes; porém, nem todos os deprimidos apresentam esta alteração na função hipotálamo-pituitária-adrenal. Os primeiros estudos publicados observaram esta hiperativação do eixo hipotálamo-pituitária-adrenal por meio do teste de supressão da dexametasona. Estes resultados não foram largamente replicados em grande parte devido à falta de acurácia desse teste. A hipercortisolemia ocorre freqüentemente em pacientes com depressão grave, do tipo melancólico, psicóticos ou não. Está relacionada a um polimorfismo específico do gene do transportador da serotonina; a história de abuso ou negligência durante a infância ou perda parental precoce; e ao temperamento que resulta em alterações na resposta ao estresse. CONCLUSÕES: As alterações do eixo hipotálamo-pituitária-adrenal dependem de diversos fatores, como gravidade e tipo de depressão, genótipo, história de trauma na infância, temperamento e, provavelmente, resiliência. Todas essas variáveis se relacionam a um endofenótipo vulnerável ao desenvolvimento de depressão.


OBJECTIVE: To review the new findings about stress, hypothalamic-pituitary-adrenal axis and depression trying to explain a possible endophenotype prone to depression. METHOD: Nonsystematic review of the literature based on the endophenotype hypothesis. RESULTS: Depression is linked to hypercortisolemia in many patients, but not all patients present these hypothalamic-pituitary-adrenal axis dysfunction. The dexamethasone suppression test is not the most accurate test to measure the hypothalamic-pituitary-adrenal axis function, and its use in the first studies published probably jeopardized the results. Hypercortisolemia frequently occurs in patients with severe depression, melancholic, either psychotic or nonpsychotic type; it is linked to the presence of a polymorphism in the promoter of the serotonin transporter gene, with a history of childhood abuse or neglect, or other significant stressful experiences like the loss of a parent during childhood and temperament leading to alterations in the response to stress. CONCLUSIONS: The alterations of the hypothalamic-pituitary-adrenal axis depend on many factors like severity and type of depression, genotype, history of exposure to stress, temperament, and probably resilience. All these factors together result in an endophenotype thought to be prone to depression.


Subject(s)
Humans , Depressive Disorder, Major/genetics , Glucocorticoids/metabolism , Hypothalamo-Hypophyseal System/physiopathology , Pituitary-Adrenal System/physiopathology , Stress, Psychological/genetics , Adrenocorticotropic Hormone/metabolism , Corticotropin-Releasing Hormone , Depressive Disorder, Major/physiopathology , Dexamethasone , Genetic Predisposition to Disease , Phenotype , Polymorphism, Genetic , Stress, Psychological/physiopathology , Temperament
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