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.

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.

Abstract 17: Early Life Stress Sensitizes The Angiotensin II-elicited Hypertensive Response

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Baojian Xue ◽  
Terry Beltz ◽  
Fang Guo ◽  
David M Pollock ◽  
Jennifer S Pollock ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Proinflammatory Cytokines ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Male Rats ◽  
Sprague Dawley ◽  
Cns Inflammation ◽  
Wide Range ◽  
The Brain

Separation of neonatal rodent pups from their mothers has been used as a model to study the effects of early life stress (ELS) on behavioral and physiological responses in adults. Using an Induction-Delay-Expression experimental paradigm, our previous studies demonstrate that a wide range of stressors administered during an induction period produces hypertensive response sensitization (HTRS) in response to a subsequent pro-hypertensive stimulus. HTRS is accompanied by activation of the brain renin-angiotensin system (RAS) and CNS inflammation. The present study investigated whether ELS induces HTRS and changes in brain-related underlying mechanisms. Rat neonates from Sprague-Dawley breeders were subjected to ELS by separating them each morning from their mothers for 3 h on postnatal days 2 to 14. Pups from non-handled litters formed control groups. At 10 weeks of age, male rats were used to evaluate blood pressure and autonomic function using telemetric probes and pharmacological methods. In addition, in separate control and ELS groups, the lamina terminalis (LT) structures and the hypothalamic paraventricular nucleus (PVN) were analyzed for mRNA expression of RAS components and proinflammatory cytokines. Adult ELS rats as compared to non-separated controls exhibited 1) HTRS during expression testing using 2 week ANG II infusions (120 ng/kg/min s.c.; ELS animals, Δ45.5±4.5 mmHg vs. controls, Δ22.4±3.1 mmHg); 2) a greater reduction in mean arterial pressure following ganglionic blockade (hexamethonium, 30 mg/kg, ip), 3) increased sympathetic drive to the heart (atenolol, 8 mg/kg, ip), 4) decreased vagal tone (atropine, 8 mg/kg, ip), and 5) increased mRNA expression of several components of the brain RAS and proinflammatory cytokines in the LT and PVN. These results suggest that maternal ELS may predispose individuals to hypertension that is mediated by upregulation of the brain RAS and proinflammatory cytokines and increased sympathetic drive to the cardiovascular system.

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

Early Life Stress: Long-Term Physiological Impact in Rodents and Primates

Physiology ◽  
2002 ◽  
Vol 17 (4) ◽  
pp. 150-155 ◽  
Author(s):  
Christopher R. Pryce ◽  
Daniela Rüedi-Bettschen ◽  
Andrea C. Dettling ◽  
Joram Feldon
Keyword(s):  
Life Span ◽  
Stress Responses ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Human Infants ◽  
Hypothalamic Pituitary Adrenal ◽  
Physiological Impact ◽  
Pituitary Adrenal Axis

Rat, monkey, and human infants have evolved to expect certain patterns of care. Spontaneous or experimental deviations of care from the norm result in infant stress responses. Hyperactivity of immature stress systems such as the limbic-hypothalamic-pituitary-adrenal axis and the limbic-sympatho-adrenomedullary axis can alter their subsequent reactivity across the life span.

scholarly journals Instrumental Learning and Cognitive Flexibility Processes are Impaired in Children Exposed to Early Life Stress

2020 ◽  
Author(s):  
Madeline Harms ◽  
Katherine Shannon Bowen ◽  
Jamie Lars Hanson ◽  
Seth Pollak
Keyword(s):  
Cognitive Flexibility ◽  
Life Stress ◽  
Early Life ◽  
Instrumental Learning ◽  
Early Life Stress ◽  
Social Adaptation ◽  
Neural Activation ◽  
Learning Mechanisms ◽  
Early Stress ◽  
Brain Circuitry

Children who experience severe early life stress show persistent deficits in many aspects of cognitive and social adaptation. Early stress might be associated with these broad changes in functioning because it impairs general learning mechanisms. To explore this possibility, we examined whether individuals who experienced abusive caregiving in childhood had difficulties with instrumental learning and/or cognitive flexibility as adolescents. Fifty‐three 14–17‐year‐old adolescents (31 exposed to high levels of childhood stress, 22 control) completed an fMRI task that required them to first learn associations in the environment and then update those pairings. Adolescents with histories of early life stress eventually learned to pair stimuli with both positive and negative outcomes, but did so more slowly than their peers. Furthermore, these stress‐exposed adolescents showed markedly impaired cognitive flexibility; they were less able than their peers to update those pairings when the contingencies changed. These learning problems were reflected in abnormal activity in learning‐ and attention‐related brain circuitry. Both altered patterns of learning and neural activation were associated with the severity of lifetime stress that the adolescents had experienced. Taken together, the results of this experiment suggest that basic learning processes are impaired in adolescents exposed to early life stress. These general learning mechanisms may help explain the emergence of social problems observed in these individuals.

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.

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