scholarly journals For better or worse: reduced adult lifespan following early-life stress is transmitted to breeding partners

2011 ◽  
Vol 279 (1729) ◽  
pp. 709-714 ◽  
Author(s):  
Pat Monaghan ◽  
Britt J. Heidinger ◽  
Liliana D'Alba ◽  
Neil P. Evans ◽  
Karen A. Spencer
Keyword(s):  
Stress Responses ◽  
Life Stress ◽  
Disease Risk ◽  
Stress Hormones ◽  
Adult Life ◽  
Early Life Stress ◽  
Stress Sensitivity ◽  
Adult Lifespan ◽  
Early Stress ◽  
Negative Effect

Stressful conditions early in life can give rise to exaggerated stress responses, which, while beneficial in the short term, chronically increase lifetime exposure to stress hormones and elevate disease risk later in life. Using zebra finches Taeniopygia guttata , we show here that individuals whose glucocorticoid stress hormones were experimentally increased for only a brief period in early post-natal life, inducing increased stress sensitivity, had reduced adult lifespans. Remarkably, the breeding partners of such exposed individuals also died at a younger age. This negative effect on partner longevity was the same for both sexes; it occurred irrespective of the partner's own early stress exposure and was in addition to any longevity reduction arising from this. Furthermore, this partner effect continued even after the breeding partnership was terminated. Only 5 per cent of control birds with control partners had died after 3 years, compared with over 40 per cent in early stress–early stress pairs. In contrast, reproductive capability appeared unaffected by the early stress treatment, even when breeding in stressful environmental circumstances. Our results clearly show that increased exposure to glucocorticoids early in life can markedly reduce adult life expectancy, and that pairing with such exposed partners carries an additional and substantial lifespan penalty.

The adaptive and maladaptive continuum of stress responses – a hippocampal perspective

2015 ◽  
Vol 26 (4) ◽  
Author(s):  
Deepika Suri ◽  
Vidita A. Vaidya
Keyword(s):  
Stress Responses ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Negative Consequences ◽  
Functional Responses ◽  
Physiological Level ◽  
Early Stress ◽  
Wide Range ◽  
Potential Factors

AbstractExposure to stressors elicits a spectrum of responses that span from potentially adaptive to maladaptive consequences at the structural, cellular and physiological level. These responses are particularly pronounced in the hippocampus where they also appear to influence hippocampal-dependent cognitive function and emotionality. The factors that influence the nature of stress-evoked consequences include the chronicity, severity, predictability and controllability of the stressors. In addition to adult-onset stress, early life stress also elicits a wide range of structural and functional responses, which often exhibit life-long persistence. However, the outcome of early stress exposure is often contingent on the environment experienced in adulthood, and could either aid in stress coping or could serve to enhance susceptibility to the negative consequences of adult stress. This review comprehensively examines the consequences of adult and early life stressors on the hippocampus, with a focus on their effects on neurogenesis, neuronal survival, structural and synaptic plasticity and hippocampal-dependent behaviors. Further, we discuss potential factors that may tip stress-evoked consequences from being potentially adaptive to largely maladaptive.

scholarly journals Early embryonic heat shock induces long-term epigenetic memory by affecting the transition to zygotic independence

2021 ◽  
Author(s):  
Lovisa Örkenby ◽  
Signe Skog ◽  
Helen Ekman ◽  
Unn Kugelberg ◽  
Rashmi Ramesh ◽  
...  
Keyword(s):  
Heat Shock ◽  
Life Stress ◽  
Disease Risk ◽  
Early Life Stress ◽  
Stress Sensitivity ◽  
Adult Health ◽  
Strong Negative Correlation ◽  
Epigenetic Alteration ◽  
Non Coding Rna

Early-life stress can generate persistent life-long effects that impact adult health and disease risk, but little is known of how such programming is established and maintained. Previous use of the Drosophila strain wm4h show that an early embryonic heat shock result in stable epigenetic alteration in the adult fly. To investigate the potential role of small non-coding RNA (sncRNA) in the initiation of such long-term epigenetic effects, we here generated a fine timeline of sncRNA expression during the first 5 stages of Drosophila embryogenesis in this strain. Building on this, we show that (1) miRNA is increased following early embryonic heat shock, and (2) the increased miRNA is coming from two separate sources, maternal and zygotic. By performing long RNA sequencing on the same single embryo, we found that a subgroup of miRNA with maternal origin, had a strong negative correlation with a group of early zygotic transcripts. Critically, we found evidence that one such early zygotic transcript, the insulator binding factor Elba1, is a Su(var) for wm4h. The findings provide insights of the dynamics and stress-sensitivity of sncRNA during the first embryonic stages in Drosophila and suggest an interplay between miRNA, Elba1 and long-term epigenetic alteration.

Connect-the-DOT from early stress to depression

2021 ◽  
Vol 14 (678) ◽  
pp. eabi9138
Author(s):  
Leslie K. Ferrarelli
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Behavioral Effects ◽  
Early Stress

Targeting the epigenetic enzyme DOT1L may reverse some behavioral effects of early-life stress.

scholarly journals Impaired developmental microglial pruning of excitatory synapses on CRH-expressing hypothalamic neurons exacerbates stress responses throughout life

2021 ◽  
Author(s):  
Jessica L Bolton ◽  
Annabel K Short ◽  
Shivashankar Othy ◽  
Cassandra L Kooiker ◽  
Manlin Shao ◽  
...  
Keyword(s):  
Stress Responses ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Mental Illnesses ◽  
Excitatory Synapses ◽  
Process Dynamics ◽  
Brain Circuits ◽  
Synapse Density ◽  
And Function

The developmental origins of stress-related mental illnesses are well-established, and early-life stress/adversity (ELA) is an important risk factor. However, it is unclear how ELA impacts the maturation of salient brain circuits, provoking enduring vulnerability to stress and stress-related disorders. Here we find that ELA increases the number and function of excitatory synapses onto stress-sensitive hypothalamic corticotropin-releasing hormone (CRH)-expressing neurons, and implicate disrupted synapse pruning by microglia as a key mechanism. Microglial process dynamics on live imaging, and engulfment of synaptic elements by microglia, were both attenuated in ELA mice, associated with deficient signaling of the microglial phagocytic receptor Mer. Accordingly, selective chemogenetic activation of ELA microglia increased microglial process dynamics and reduced excitatory synapse density to control levels. Selective early-life microglial activation also mitigated the adrenal hypertrophy and prolonged stress responses in adult ELA mice, establishing microglial actions during development as powerful contributors to experience-dependent sculpting of stress-related brain circuits.

scholarly journals Early life stress alters transcriptomic patterning across reward circuitry in male and female mice

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Catherine Jensen Peña ◽  
Milo Smith ◽  
Aarthi Ramakrishnan ◽  
Hannah M. Cates ◽  
Rosemary C. Bagot ◽  
...  
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Cortical Plasticity ◽  
Early Life Stress ◽  
Stress Sensitivity ◽  
Sensitive Period ◽  
Male And Female ◽  
Reward Circuitry ◽  
Female Mice ◽  
Increase Risk

Abstract Abuse, neglect, and other forms of early life stress (ELS) significantly increase risk for psychiatric disorders including depression. In this study, we show that ELS in a postnatal sensitive period increases sensitivity to adult stress in female mice, consistent with our earlier findings in male mice. We used RNA-sequencing in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of male and female mice to show that adult stress is distinctly represented in the brain’s transcriptome depending on ELS history. We identify: 1) biological pathways disrupted after ELS and associated with increased behavioral stress sensitivity, 2) putative transcriptional regulators of the effect of ELS on adult stress response, and 3) subsets of primed genes specifically associated with latent behavioral changes. We also provide transcriptomic evidence that ELS increases sensitivity to future stress through enhancement of known programs of cortical plasticity.

scholarly journals Early Life Stress Restricts Translational Reactivity in CA3 Neurons Associated With Altered Stress Responses in Adulthood

2019 ◽  
Vol 13 ◽  
Author(s):  
Jordan Marrocco ◽  
Jason D. Gray ◽  
Joshua F. Kogan ◽  
Nathan R. Einhorn ◽  
Emma M. O’Cinneide ◽  
...  
Keyword(s):  
Stress Responses ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Ca3 Neurons

scholarly journals Human amygdala engagement moderated by early life stress exposure is a biobehavioral target for predicting recovery on antidepressants

2016 ◽  
Vol 113 (42) ◽  
pp. 11955-11960 ◽  
Author(s):  
Andrea N. Goldstein-Piekarski ◽  
Mayuresh S. Korgaonkar ◽  
Erin Green ◽  
Trisha Suppes ◽  
Alan F. Schatzberg ◽  
...  
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Controlled Trial ◽  
Stress Hormones ◽  
Early Life Stress ◽  
Emotional Stimuli ◽  
Response To Stress ◽  
The Individual ◽  
Human Neuroimaging ◽  
Amygdala Reactivity

Amygdala circuitry and early life stress (ELS) are both strongly and independently implicated in the neurobiology of depression. Importantly, animal models have revealed that the contribution of ELS to the development and maintenance of depression is likely a consequence of structural and physiological changes in amygdala circuitry in response to stress hormones. Despite these mechanistic foundations, amygdala engagement and ELS have not been investigated as biobehavioral targets for predicting functional remission in translational human studies of depression. Addressing this question, we integrated human neuroimaging and measurement of ELS within a controlled trial of antidepressant outcomes. Here we demonstrate that the interaction between amygdala activation engaged by emotional stimuli and ELS predicts functional remission on antidepressants with a greater than 80% cross-validated accuracy. Our model suggests that in depressed people with high ELS, the likelihood of remission is highest with greater amygdala reactivity to socially rewarding stimuli, whereas for those with low-ELS exposure, remission is associated with lower amygdala reactivity to both rewarding and threat-related stimuli. This full model predicted functional remission over and above the contribution of demographics, symptom severity, ELS, and amygdala reactivity alone. These findings identify a human target for elucidating the mechanisms of antidepressant functional remission and offer a target for developing novel therapeutics. The results also offer a proof-of-concept for using neuroimaging as a target for guiding neuroscience-informed intervention decisions at the level of the individual person.

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