Impacts of stress on reproductive and social behaviors

Magariños, Ana Marı́a; Schaafsma, Sara M.; Pfaff, Donald W.

doi:10.1016/j.yfrne.2018.01.002

Cited by 8 publications

(4 citation statements)

References 52 publications

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“…Finally, prenatal stress and ELS are risk factors for ASD ( Beversdorf et al, 2018 ; Magariños et al, 2018 ). Epigenetic alterations provoked by prenatal stress and/or ELS exposure may play a central role in the long-term biological trajectories of ASD, mainly through the disruption of developmental programming of stress related structural and molecular neurobiological pathways ( Cattane et al, 2020 ; Panisi et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Early life stress has been recognized as a key mediator of developmental programming, since a limited insult during developmental vulnerability windows may increase the risk for either subclinical neuropsychological alterations or clinical conditions, such as neurodevelopmental disorders ( Reynolds et al, 2013 ; Ghiani and Faundez, 2017 ; Pervanidou et al, 2017 ). It has been suggested that ELS, precisely prenatal maternal stress (PMS) and infant stress, is a risk factor for ASD ( Beversdorf et al, 2018 ; Magariños et al, 2018 ). In fact, the embryo-fetal period and infancy are the most vulnerable periods of brain development ( Kuhlman et al, 2017 ; Panisi et al, 2021 ).…”

Section: Stress System Developmental Trajectory and The Role Of Early Life Stressmentioning

confidence: 99%

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Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

et al. 2022

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The mission of the human stress system is the maintenance of homeostasis in the presence of real or perceived, acute or chronic stressors. The hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS) are the stress system-related neuroendocrine pathways. There is abundant evidence that children and adolescents with autism spectrum disorder (ASD) may exhibit atypical function within the HPA axis and the ANS both at the resting state and during the presence of social and/or non-social stressors. The aim of this review is to provide an up-to-date summary of the findings regarding stress system alterations in children and adolescents with ASD. We focus on the variations of stress hormones circadian rhythms, specifically cortisol and alpha-amylase (i.e., a surrogate index of epinephrine/norepinephrine secretion), and on the alterations of stress system responsivity to different stressors. Also, we present imaging and immunological findings that have been associated with stress system dysregulation in children and adolescents with ASD. Finally, we review the pivotal role of HPA axis-ANS coordination, the developmental trajectory of the stress system in ASD, and the possible role of early life stress in the dysregulation of the stress system demonstrated in children and adolescents with ASD. This synthesis will hopefully provide researchers with a foundation for an integrated approach to future research into stress system variations in children and adolescents with ASD.

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Section: Discussionmentioning

confidence: 99%

Section: Stress System Developmental Trajectory and The Role Of Early Life Stressmentioning

confidence: 99%

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

et al. 2022

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“…В настоящее время особый интерес представляют научные работы, отражающие результаты изучения патологического влияния стрессогенных факторов, в том числе и «социального» стресса, на различные системы организма [1,2]. Исследования последних лет доказывают тот факт, что длительное воздействие стресса способствует формированию неврологических, иммунных, эндокринных, оксидантных, метаболических и других видов расстройств, что в конечном итоге, приводит к развитию нарушений молекулярно-клеточных механизмов запрограммированной гибели клеток, в том числе и апоптоза нейронов [3,4]. На сегодняшний день пристальное внимание уделяется оценке роли апоптотических и нейротрофических факторов в реализации стрессовой реакции.…”

Section: Introductionunclassified

Effect of Glyprolines on the Level of Apoptotic and Neurotrophic Factors Under Conditions of “Social” Stress

Ясенявская

Цибизова

Andreeva

et al. 2021

Farm. farmakol. (Pâtigorsk)

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The aim of the article was to study the effect of glyproline neuropeptide compounds Thr–Lys–Pro–Arg–Pro–Gly–Pro (Selank), Pro–Gly–Pro and Pro–Gly–Pro–Leu, on the level of apoptotic factors (caspase-3, caspase-8, the tumor necrosis factor) and neurotrophic factors (the nerve growth factor and the brain neurotrophic factor) in the blood serum of white rats under the experimental modeling of “social” stress.Materials and methods. The experimental studies were carried out on 90 nonlinear white male rats aged 6 months. By the type of behavior, in the process of “social” stress modeling, all the rats were divided into “aggressors” and “victims”. In the study, the following experimental groups (n=10) were formed: control individuals; groups of the rats exposed to stress for 20 days; groups of the animals treated intraperitoneally at the dose of 100 μg/kg/day, starting from the 1st day of the stress factor exposure, with a course of 20 days of glyproline compounds Thr–Lys–Pro–Arg–Pro–Gly–Pro (Selank), Pro–Gly–Pro and Pro–Gly–Pro–Leu. The effect of the compounds on the level of apoptotic and neurotrophic factors was assessed by determining the level of caspase-3, caspase-8, the tumor necrosis factor, the nerve growth factor and the brain neurotrophic factor of white rat blood serum by enzyme immunoassay.Results. According to the results of the study, it was found out that under the conditions of “social” stress, there was an increase in the apoptotic processes accompanied by an increase in the level of caspase-3, caspase-8, TNF-α in the blood serum of white rats, as well as a decrease in the concentration of neurotrophic factors – BDNF and NGF. The administration of giproline compounds against the background of stress, contributed to the restoration of the studied indicators level, which is most likely due to the presence of antiapoptotic and neuroprotective effects in giprolines due to the inhibition of the caspase-dependent cascade of apoptosis reactions, as well as the induction of the synthesis of neurotrophic factors with the antiapoptotic activity.Conclusion. Thus, the administration of glyproline neuropeptide compounds Thr–Lys–Pro–Arg–Pro–Gly–Pro (Selank), Pro–Gly–Pro and Pro–Gly–Pro–Leu under stress conditions, contributes to the restoration of the initiating and effector caspases level, as well as of neurotrophic factors. As a result of the experiment, an anti-apoptotic effect is observed due to the inhibition of the caspase-dependent cascade of reactions, as well as a stress-protective effect is observed due to the restoration of the brain neurotrophic factors level.

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“…There is support in the literature for altered BDNF in humans with depression (Lee and Kim, 2010 ; Zaletel et al, 2017 ) and anxiety (Soliman et al, 2010 ; Castrén, 2014 ). Stress has been recognized as a major environmental risk factor in the pathophysiology of schizophrenia models (van Os et al, 2010 ; Brown, 2011 ; Magariños et al, 2018 ), and depression and anxiety (Binder and Nemeroff, 2010 ; Zaletel et al, 2017 ). We therefore modeled the “two-hit” hypothesis by combining genetic haploinsufficiency in the BDNF gene (1st hit) with adolescent chronic corticosterone treatment (2nd hit).…”

Section: Introductionmentioning

confidence: 99%

Sex-Dependent Effects of Environmental Enrichment on Spatial Memory and Brain-Derived Neurotrophic Factor (BDNF) Signaling in a Developmental “Two-Hit” Mouse Model Combining BDNF Haploinsufficiency and Chronic Glucocorticoid Stimulation

Grech

Ratnayake

Hannan

et al. 2018

Front. Behav. Neurosci.

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Neurodevelopmental disorders are thought to be caused by a combination of adverse genetic and environmental insults. The “two-hit” hypothesis suggests that an early first “hit” primes the developing brain to be vulnerable to a second “hit” during adolescence which triggers behavioral dysfunction. We have previously modeled this scenario in mice and found that the combined effect of a genetic hapolinsuffuciency in the brain-derived neurotrophic factor (BDNF) gene (1st hit) and chronic corticosterone (CORT) treatment during adolescence (2nd hit), caused spatial memory impairments in adulthood. Environmental enrichment (EE) protocols are designed to stimulate experience-dependent plasticity and have shown therapeutic actions. This study investigated whether EE can reverse these spatial memory impairments. Wild-type (WT) and BDNF heterozygous (HET) mice were treated with corticosterone (CORT) in their drinking water (50 mg/L) from weeks 6 to 8 and exposed to EE from 7 to 9 weeks. Enriched housing included open top cages with additional toys, tunnels, housing, and platforms. Y-maze novel preference testing, to assess short-term spatial memory, was performed at 10 weeks of age. At week 16 dorsal hippocampus tissue was obtained for Western blot analysis of expression levels of BDNF, the BDNF receptor TrkB, and NMDA receptor subunits, GluNR1, 2A and 2B. As in our previous studies, spatial memory was impaired in our two-hit (BDNF HET + CORT) mice. Simultaneous EE prevented these impairments. However, EE appeared to worsen spatial memory performance in WT mice, particularly those exposed to CORT. While BDNF levels were lower in BDNF HET mice as expected, there were no further effects of CORT or EE in males but a close to significant female CORT × EE × genotype interaction which qualitatively corresponded with Y-maze performance. However, EE caused both sex- and genotype-specific effects on phosphorylated TrkB residues and GluNR expression within the dorsal hippocampus, with GluNR2B levels in males changing in parallel with spatial memory performance. In conclusion, beneficial effects of EE on spatial memory emerge only following two developmental disruptions. The mechanisms by which EE exerts its effects are likely via regulation of multiple activity-dependent pathways, including TrkB and NMDA receptor signaling.

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Impacts of stress on reproductive and social behaviors

Cited by 8 publications

References 52 publications

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

Effect of Glyprolines on the Level of Apoptotic and Neurotrophic Factors Under Conditions of “Social” Stress

Sex-Dependent Effects of Environmental Enrichment on Spatial Memory and Brain-Derived Neurotrophic Factor (BDNF) Signaling in a Developmental “Two-Hit” Mouse Model Combining BDNF Haploinsufficiency and Chronic Glucocorticoid Stimulation

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