Prenatal Stress and Stress Coping Style Interact to Predict Metabolic Risk in Male Rats

Boersma, Gretha J.; Moghadam, Alexander A.; Cordner, Zachary A.; Tamashiro, Kellie L.K.

doi:10.1210/en.2013-1874

Cited by 19 publications

(15 citation statements)

References 34 publications

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“…In our recent studies, we found that PNS may modulate the stress-coping phenotype of the offspring. We showed that the distribution of the stress-coping behavior, expressed as the percentage time spent burying during the defensive burying test, was altered within the PNS rat population ( Boersma et al., 2014a ). In contrast to the control population, where about 16% of the rats were characterized as intermediate, there were no rats showing an intermediate stress-coping phenotype within the PNS offspring population ( Fig.…”

Section: Individual Differences – Susceptibility and Resiliencementioning

confidence: 99%

Individual differences in the effects of prenatal stress exposure in rodents

Boersma

Tamashiro

2015

Neurobiology of Stress

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Exposure to prenatal stress alters the phenotype of the offspring in adulthood. When the prenatal and adult environments do not match, these alterations may induce pathology risk. There are, however, large individual differences in the effects of prenatal stress. While some individuals seem vulnerable, others appear to be relatively resistant to its effects. In this review we discuss potential mechanisms underlying these individual differences with a focus on animal models. Differences between rodent models selected for stress coping traits are discussed. In addition, the role of circulating factors, like glucocorticoids and cytokines, factors involved in brain development and influences of epigenetic and genetic factors in prenatal stress induced phenotype are covered.

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Section: Individual Differences – Susceptibility and Resiliencementioning

confidence: 99%

Individual differences in the effects of prenatal stress exposure in rodents

Boersma

Tamashiro

2015

Neurobiology of Stress

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“…Conversely, MS180 is a model of chronic postnatal stress that involves separating the pups from their mother for periods of 3 hr each day during the first 2 weeks of life (van Bodegom et al, 2017;Lehmann & Feldon, 2000;Meaney et al, 1996;Tractenberg et al, 2016). As adults, PNS and MS180 rats present a large repertoire of pathologies that include increased emotionality (Lajud, Roque, Cajero, Gutiérrez-Ospina, & Torner, 2012;Marrocco et al, 2014;Veenema, Blume, Niederle, Buwalda, & Neumann, 2006; Marta Weinstock, 2017) and metabolic risk (Boersma, Moghadam, Cordner, & Tamashiro, 2014;Ruiz et al, 2018;Vargas, Junco, Gomez, & Lajud, 2016). Recent evidence from our laboratory indicated that while MS180 increases baseline GC levels, it has no effect on the HPA axis response to a physical stressor; however, MS180 affects GC response to fasting (Ruiz et al, 2018).…”

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confidence: 99%

Prenatal immobilization stress and postnatal maternal separation cause differential neuroendocrine responses to fasting stress in adult male rats

Roque

Ruiz‐González

Pineda-López

et al. 2019

Developmental Psychobiology

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Prenatal immobilization stress (PNS) and postnatal maternal separation (MS180) are two widely used rodent models of early‐life stress (ELS) that affect the hypothalamus–pituitary–adrenal (HPA) axis, cause behavioral alterations, and affect glucose tolerance in adults. We compared anxiety‐like behavior, coping strategies, and HPA axis activity in PNS and MS180 adult (4‐month‐old) male rats and assessed their glucose tolerance and HPA axis response after mild fasting stress. Both PNS and MS180 induced a passive coping strategy in the forced swimming test, without affecting anxiety‐like behavior in the elevated plus‐maze. Moreover, both PNS and MS180 increased the hypothalamic corticotropin‐releasing hormone expression; however, only MS180 increased the circulating corticosterone levels. Both early life stressors increased fasting glucose levels and this effect was significantly higher in PNS rats. MS180 rats showed impaired glucose tolerance 120 min after intravenous glucose administration, whereas PNS rats displayed an efficient homeostatic response. Moreover, MS180 rats showed higher circulating corticosteroid levels in response to fasting stress (overnight fasting, 12 hr), which were restored after glucose administration. In conclusion, early exposure to postnatal MS180, unlike PNS, increases the HPA axis response to moderate fasting stress, indicating a differential perception of fasting as a stressor in these two ELS models.

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“…The shock probe burying test was used to characterize defensive behavior and coping style (Boersma et al, 2014). Rats were placed in a novel shoebox cage with clean bedding for 10 min of habituation.…”

Section: Shock Probe Defensive Buryingmentioning

confidence: 99%

Infralimbic cortical glutamate output is necessary for the neural and behavioral consequences of chronic stress

Pace

Christensen

Schackmuth

et al. 2020

Preprint

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AbstractExposure to prolonged stress is a major risk-factor for psychiatric disorders such as generalized anxiety and major depressive disorder (MDD). Human imaging studies have identified structural and functional abnormalities in the prefrontal cortex of MDD patients, particularly Brodmann’s area 25 (BA25). Further, deep brain stimulation of BA25 reduces symptoms of treatment-resistant depression. The rat homolog of BA25 is the infralimbic cortex (IL), which is critical for cognitive appraisal, executive function, and physiological stress reactivity. Previous studies indicate that the IL undergoes stress-induced changes in excitatory/inhibitory balance culminating in reduced activity of glutamate output neurons. However, the regulatory role of IL glutamate output in mood-related behaviors after chronic variable stress (CVS) is unknown. Here, we utilized a lentiviral-packaged small-interfering RNA to reduce translation of vesicular glutamate transporter 1 (vGluT1 siRNA), thereby constraining IL glutamate output. This viral-mediated gene transfer was used in conjunction with a quantitative anatomical analysis of cells expressing the stable immediate-early gene product ΔFosB, which accumulates in response to repeated neural activation. Through assessment of ΔFosB-expressing neurons across the frontal lobe in adult male rats, we mapped regions altered by chronic stress and determined the coordinating role of the IL in frontal cortical plasticity. Specifically, CVS-exposed rats had increased density of ΔFosB-expressing cells in the IL and decreased density in the anterior insula. The later effect was dependent on IL glutamate output. Next, we examined the interaction of CVS and reduced IL glutamate output in behavioral assays examining coping, anxiety-like behavior, associative learning, and nociception. IL glutamate knockdown decreased immobility during the forced swim test compared to GFP controls, both in rats exposed to CVS as well as rats without previous stress exposure. Further, vGluT1 siRNA prevented CVS-induced avoidance behaviors, while also reducing risk aversion and passive coping. Ultimately, this study identifies the necessity of IL glutamatergic output for regulating frontal cortical neural activity and behavior following chronic stress. These findings also highlight how disruption of excitatory/inhibitory balance within specific frontal cortical cell populations may impact neurobehavioral adaptation and lead to stress-related disorders.

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Prenatal Stress and Stress Coping Style Interact to Predict Metabolic Risk in Male Rats

Cited by 19 publications

References 34 publications

Individual differences in the effects of prenatal stress exposure in rodents

Individual differences in the effects of prenatal stress exposure in rodents

Prenatal immobilization stress and postnatal maternal separation cause differential neuroendocrine responses to fasting stress in adult male rats

Infralimbic cortical glutamate output is necessary for the neural and behavioral consequences of chronic stress

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