The effect of different maternal deprivation paradigms on the expression of hippocampal glucocorticoid receptors, calretinin and calbindin-D28k in male and female adolescent rats

Xu, Hao; Hu, Wendong; Zhang, Xuesi; Gao, Wei; Ming, Liang; Chen, Tao; He, Xiaosheng; Hu, Zhian

doi:10.1016/j.neuint.2011.07.010

Cited by 13 publications

(17 citation statements)

References 39 publications

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“…An animal’s ability to respond to stress is immature at birth and the lifespan is characterized by a stress-hyporesponsive period that lasts from approximately the first to second weeks of life (Sapolsky and Meaney, 1986). Excessive stress, exposure to glucocorticoids, or prolonged absence from the dam can permanently terminate this stress hyporesponsive period, leading to life-long hypersensitivity to stress (Lehmann et al, 2002a,b; Barna et al, 2003; Xu et al, 2011). Certainly, early life stressful events such as maternal separation in the rodent, or child abuse/loss of a parent in humans can cause disruption of the HPA axis in this way (Koch et al, 2008; D’Argenio et al, 2009).…”

Section: Early Life Hpa Axis Development and Its Effects On Eating Bementioning

confidence: 99%

Eating behavior and stress: a pathway to obesity

2014

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Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body’s resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie “palatable” food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society.

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Section: Early Life Hpa Axis Development and Its Effects On Eating Bementioning

confidence: 99%

Eating behavior and stress: a pathway to obesity

2014

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“…It leads to anxiety in adulthood, affects basal plasma corticosterone and ACTH, alters GR expression in the brain, and exacerbates the corticosterone response to stress (Lehmann et al, 2002a,b; Barna et al, 2003; Xu et al, 2011). Maternal separation of this type in early life can lead to a life-long reduction in food intake and a significant aversion to foods high in carbohydrates, compared with no maternal separation (Penke et al, 2001).…”

Section: Early Life Stress Programs the Hypothalamic-pituitary-adrenamentioning

confidence: 99%

Perinatal programming of neuroendocrine mechanisms connecting feeding behavior and stress

Spencer¹

2013

Front. Neurosci.

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Feeding behavior is closely regulated by neuroendocrine mechanisms that can be influenced by stressful life events. However, the feeding response to stress varies among individuals with some increasing and others decreasing food intake after stress. In addition to the impact of acute lifestyle and genetic backgrounds, the early life environment can have a life-long influence on neuroendocrine mechanisms connecting stress to feeding behavior and may partially explain these opposing feeding responses to stress. In this review I will discuss the perinatal programming of adult hypothalamic stress and feeding circuitry. Specifically I will address how early life (prenatal and postnatal) nutrition, early life stress, and the early life hormonal profile can program the hypothalamic-pituitary-adrenal (HPA) axis, the endocrine arm of the body's response to stress long-term and how these changes can, in turn, influence the hypothalamic circuitry responsible for regulating feeding behavior. Thus, over- or under-feeding and/or stressful events during critical windows of early development can alter glucocorticoid (GC) regulation of the HPA axis, leading to changes in the GC influence on energy storage and changes in GC negative feedback on HPA axis-derived satiety signals such as corticotropin-releasing-hormone. Furthermore, peripheral hormones controlling satiety, such as leptin and insulin are altered by early life events, and can be influenced, in early life and adulthood, by stress. Importantly, these neuroendocrine signals act as trophic factors during development to stimulate connectivity throughout the hypothalamus. The interplay between these neuroendocrine signals, the perinatal environment, and activation of the stress circuitry in adulthood thus strongly influences feeding behavior and may explain why individuals have unique feeding responses to similar stressors.

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“…Notably, calbindin expression levels are developmentally regulated and peak during the early postnatal period in the rodent neocortex (Alcá ntara et al, 1993), when the developing brain is highly sensitive to stress exposure (Liao et al, 2014;Liu et al, 2016;Yang et al, 2015). Severely stressful experiences around this critical period, which increase the risk for psychiatric disorders later in life (Humphreys and Zeanah, 2015;Nemeroff, 2016), could alter calbindin levels and the density of calbindin-positive neurons in the hippocampus (Giachino et al, 2007;Seidel et al, 2008;Xu et al, 2011) and other stress-related brain regions (Gos et al, 2014;Helmeke et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Suppressed Calbindin Levels in Hippocampal Excitatory Neurons Mediate Stress-Induced Memory Loss

Xie

et al. 2017

Cell Reports

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Calbindin modulates intracellular Ca dynamics and synaptic plasticity. Reduction of hippocampal calbindin levels has been implicated in early-life stress-related cognitive disorders, but it remains unclear how calbindin in distinct populations of hippocampal neurons contributes to stress-induced memory loss. Here we report that early-life stress suppressed calbindin levels in CA1 and dentate gyrus (DG) neurons, and calbindin knockdown in adult CA1 or DG excitatory neurons mimicked early-life stress-induced memory loss. In contrast, calbindin knockdown in CA1 interneurons preserved long-term memory even after an acute stress challenge. These results indicate that the dysregulation of calbindin in hippocampal excitatory, but not inhibitory, neurons conveys susceptibility to stress-induced memory deficits. Moreover, calbindin levels were downregulated by early-life stress through the corticotropin-releasing hormone receptor 1-nectin3 pathway, which in turn reduced inositol monophosphatase levels. Our findings highlight calbindin as a molecular target of early-life stress and an essential substrate for memory.

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The effect of different maternal deprivation paradigms on the expression of hippocampal glucocorticoid receptors, calretinin and calbindin-D28k in male and female adolescent rats

Cited by 13 publications

References 39 publications

Eating behavior and stress: a pathway to obesity

Eating behavior and stress: a pathway to obesity

Perinatal programming of neuroendocrine mechanisms connecting feeding behavior and stress

Suppressed Calbindin Levels in Hippocampal Excitatory Neurons Mediate Stress-Induced Memory Loss

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