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      Perinatal stress: characteristics and effects on adult eating behavior Translated title: Estresse peri-natal: suas características e repercussões sobre o comportamento alimentar na vida adulta

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          Abstract

          Many studies have pointed out the importance of mother-child interaction in the early months of life. A few decades ago, a method called kangaroo care was developed and its main goal was to keep underweight or premature newborns in direct contact with the mother. This method has reduced the morbidity and mortality of these newborns, increasing their growth rate, breastfeeding time and mother-child contact. In rodents, the dam's presence is crucial for avoiding aggression factors that may trigger phenotypic adaptations in the pups with irreversible morphological, functional and behavioral consequences. Eating behavior is an adaptive response stemming from the external environment demand and modulated by opportunities and limitations imposed by the external environment. This behavior is regulated by a complex interaction of peripheral and central mechanisms that control hunger and satiety. The hypothalamus is a brain structure that integrates central and peripheral signals to regulate energy homeostasis and body weight. The hypothalamic nucleus have orexigenic peptides, such as neuropeptide Y and the Agouti-related peptide, and anorexigenic peptides, such as cocaine and amphetamine regulated transcript and proopiomelanocortin. An innovative study of eating behavior in experimental models of neonatal stress separates the mother from the offspring during lactation. This review describes the effects of stress during the neonatal period on general physiological factors, particularly on the control of eating behavior.

          Translated abstract

          Muitos estudos têm apontado a importância da interação mãe-filho durante os primeiros meses de vida. Nas últimas décadas, foi desenvolvido um método, denominado mãe canguru, que tem como principal objetivo manter neonatos nascidos com baixo peso ou prematuros em contato direto com suas mães de forma contínua. Esse método tem reduzido a mortalidade e morbidade desses neonatos, aumentado medidas de crescimento, amamentação e contato mãe-filho. Em roedores, a presença da mãe é determinante para evitar a incidência de fatores agressores que possam desencadear adaptações fenotípicas dos filhotes com consequências morfofuncionais e comportamentais irreversíveis. O comportamento alimentar representa uma resposta adaptativa, decorrente da demanda do ambiente interno sendo modulado por oportunidades e limitações impostas pelo ambiente externo.Esse comportamento é regulado por uma interação complexa entre mecanismos periféricos e centrais que controlam a fome e a saciedade. O hipotálamo é a estrutura encefálica que integra sinais centrais e periféricos para regular a homeostase energética e o peso corporal. Nos núcleos hipotalâmicos são encontrados peptídeos orexigênicos como o neuropeptídeo Y e o peptídeo relacionado ao gene Agouti, e os anorexigênicos como o transcrito relacionado a cocaína e anfetamina e a pró-opiomelanocortina. O estudo do comportamento alimentar é inovador em modelos experimentais de estresse neonatal utilizando a separação entre mães e filhotes na fase de lactação. Esta revisão descreve os efeitos do estresse durante o período neonatal sobre aspectos fisiológicos gerais e particularmente sobre o controle do comportamento alimentar.

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          How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

          The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole.
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            The role of the hippocampus in feedback regulation of the hypothalamic-pituitary-adrenocortical axis.

            There is considerable, although not entirely consistent, evidence that the hippocampus inhibits most aspects of HPA activity, including basal (circadian nadir) and circadian peak secretion as well as the onset and termination of responses to stress. Although much of the evidence for these effects rests only on the measurement of corticosteroids, recent lesion and implant studies indicate that the hippocampus regulates adrenocortical activity at the hypothalamic level, via the expression and secretion of ACTH secretagogues. Such inhibition results largely from the mediation of corticosteroid feedback, although more work is required to determine whether the hippocampus supplies a tonic inhibitory input in the absence of corticosteroids. It must be noted that the hippocampus is not the only feedback site in the adrenocortical system, since removal of its input only reduces, but does not abolish, the efficacy of corticosteroid inhibition, and since other elements of the axis appear eventually to compensate for deficits in feedback regulation. The importance of other feedback sites is further suggested not only by the presence of corticosteroid receptors in other parts of the brain and pituitary, but also by the improved prediction of CRF levels by combined hypothalamic and hippocampal receptor occupancy. The likelihood of feedback mediated by nonhippocampal sites underscores the need for future work to characterize hippocampal influence on HPA activity in the absence of changes in corticosteroid secretion. However, despite the fact that the hippocampus is not the only feedback site, it is distinguished from most potential feedback sites, including the hypothalamus and pituitary, by its high content of both type I and II corticosteroid receptors. The hippocampus is therefore capable of mediating inhibition over a wide range of steroid levels. The low end of this range is represented by corticosteroid inhibition of basal (circadian nadir) HPA activity. The apparent type I receptor specificity of this inhibition and the elevation of trough corticosteroid levels after hippocampal damage support a role for hippocampal type I receptors in regulating basal HPA activity. It is possible that basal activity is controlled in part through hippocampal inhibition of vasopressin, since the inhibition of portal blood vasopressin correlates with lower levels of hippocampal receptor occupancy, and the expression of vasopressin by some CRF neurons is sensitive to very low corticosteroid levels. At the high end of the physiological range, stress-induced or circadian peak corticosteroid secretion correlates strongly with occupancy of the lower affinity hippocampal type II receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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              Brain corticosteroid receptor balance in health and disease.

              In this review, we have described the function of MR and GR in hippocampal neurons. The balance in actions mediated by the two corticosteroid receptor types in these neurons appears critical for neuronal excitability, stress responsiveness, and behavioral adaptation. Dysregulation of this MR/GR balance brings neurons in a vulnerable state with consequences for regulation of the stress response and enhanced vulnerability to disease in genetically predisposed individuals. The following specific inferences can be made on the basis of the currently available facts. 1. Corticosterone binds with high affinity to MRs predominantly localized in limbic brain (hippocampus) and with a 10-fold lower affinity to GRs that are widely distributed in brain. MRs are close to saturated with low basal concentrations of corticosterone, while high corticosterone concentrations during stress occupy both MRs and GRs. 2. The neuronal effects of corticosterone, mediated by MRs and GRs, are long-lasting, site-specific, and conditional. The action depends on cellular context, which is in part determined by other signals that can activate their own transcription factors interacting with MR and GR. These interactions provide an impressive diversity and complexity to corticosteroid modulation of gene expression. 3. Conditions of predominant MR activation, i.e., at the circadian trough at rest, are associated with the maintenance of excitability so that steady excitatory inputs to the hippocampal CA1 area result in considerable excitatory hippocampal output. By contrast, additional GR activation, e.g., after acute stress, generally depresses the CA1 hippocampal output. A similar effect is seen after adrenalectomy, indicating a U-shaped dose-response dependency of these cellular responses after the exposure to corticosterone. 4. Corticosterone through GR blocks the stress-induced HPA activation in hypothalamic CRH neurons and modulates the activity of the excitatory and inhibitory neural inputs to these neurons. Limbic (e.g., hippocampal) MRs mediate the effect of corticosterone on the maintenance of basal HPA activity and are of relevance for the sensitivity or threshold of the central stress response system. How this control occurs is not known, but it probably involves a steady excitatory hippocampal output, which regulates a GABA-ergic inhibitory tone on PVN neurons. Colocalized hippocampal GRs mediate a counteracting (i.e., disinhibitory) influence. Through GRs in ascending aminergic pathways, corticosterone potentiates the effect of stressors and arousal on HPA activation. The functional interaction between these corticosteroid-responsive inputs at the level of the PVN is probably the key to understanding HPA dysregulation associated with stress-related brain disorders. 5. Fine-tuning of HPA regulation occurs through MR- and GR-mediated effects on the processing of information in higher brain structures. Under healthy conditions, hippocampal MRs are involved in processes underlying integration of sensory information, interpretation of environmental information, and execution of appropriate behavioral reactions. Activation of hippocampal GRs facilitates storage of information and promotes elimination of inadequate behavioral responses. These behavioral effects mediated by MR and GR are linked, but how they influence endocrine regulation is not well understood. 6. Dexamethasone preferentially targets the pituitary in the blockade of stress-induced HPA activation. The brain penetration of this synthetic glucocorticoid is hampered by the mdr1a P-glycoprotein in the blood-brain barrier. Administration of moderate amounts of dexamethasone partially depletes the brain of corticosterone, and this has destabilizing consequences for excitability and information processing. 7. The set points of HPA regulation and MR/GR balance are genetically programmed, but can be reset by early life experiences involving mother-infant interaction. 8. (ABSTRACT TRUNCATED)
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                Author and article information

                Journal
                rn
                Revista de Nutrição
                Rev. Nutr.
                Pontifícia Universidade Católica de Campinas (Campinas, SP, Brazil )
                1415-5273
                1678-9865
                August 2013
                : 26
                : 4
                : 473-480
                Affiliations
                [01] Vitória de Santo Antão PE orgnameUniversidade Federal de Pernambuco orgdiv1Centro Acadêmico de Vitória orgdiv2Núcleo de Nutrição Brasil
                [02] Recife PE orgnameUniversidade Federal de Pernambuco orgdiv1Centro de Ciências Biológicas orgdiv2Departamento de Anatomia Brasil
                [03] Recife PE orgnameUniversidade Federal de Pernambuco orgdiv1Centro de Ciências da Saúde Brasil
                [04] Recife PE orgnameUniversidade Federal de Pernambuco orgdiv1Centro de Ciências da Saúde orgdiv2Departamento de Nutrição Brasil
                Article
                S1415-52732013000400009 S1415-5273(13)02600400009
                439daf66-d685-4a90-8f11-c6e066f08750

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 06 June 2012
                : 27 February 2013
                : 07 March 2012
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 50, Pages: 8
                Product

                SciELO Brazil

                Categories
                Review

                Stress,Estresse,Ratos,Perinatal,Comportamento alimentar,Rats,Feeding behavior

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