scholarly journals Early life adversity decreases fear expression in pre-adolescence by accelerating amygdalar parvalbumin cell development

2020 ◽  
Author(s):  
Gabriela Manzano Nieves ◽  
Marylin Bravo ◽  
Kevin G. Bath
Keyword(s):  
Emotional Regulation ◽  
Early Life ◽  
Emotional Reactivity ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Inhibitory Interneuron ◽  
Fear Learning ◽  
Early Life Adversity ◽  
Increased Risk ◽  
Fear Expression

AbstractResource insecurity (e.g., poverty) can be a significant source of stress. Decreased resources during childhood has been associated with increased risk for developing stress-related disorders, including major depressive disorder and anxiety Although the link between early life adversity and increased risk for psychopathology has been well established, the developmental mechanisms remain unclear. Using a mouse model of poverty-like rearing, limited bedding and nesting materials (LB), we tested the effects of LB on the development of fear learning and of key neuronal structures involved in emotional regulation, the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA). LB delayed the ability of pre-adolescent mice to express, but not form, an auditory conditioned fear memory. LB disrupted typical fear circuit development, accelerating parvalbumin positive (PV+) inhibitory interneuron maturation in the BLA and delaying the maturation of connections between the mPFC and BLA. The decreased fear expression in LB reared mice during early development was rescued through optogenetic inactivation of PV+ cells in the BLA. Together our data demonstrate that LB has profound and deleterious effects on mPFC and BLA development, decreasing threat-associated behavior expression, but not learning, in childhood. The current results provide a model of transiently blunt emotional reactivity in childhood, with fear-associated memories emerging later in adolescence, and possibly contributing to later pathology development.

scholarly journals Early life adversity decreases pre-adolescent fear expression by accelerating amygdala PV cell development

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Gabriela Manzano Nieves ◽  
Marilyn Bravo ◽  
Saba Baskoylu ◽  
Kevin G Bath
Keyword(s):  
Emotional Regulation ◽  
Early Life ◽  
Emotional Reactivity ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Fear Learning ◽  
Early Life Adversity ◽  
Increased Risk ◽  
Old Mice ◽  
Fear Expression

Early life adversity (ELA) is associated with increased risk for stress-related disorders later in life. The link between ELA and risk for psychopathology is well established but the developmental mechanisms remain unclear. Using a mouse model of resource insecurity, limited bedding (LB), we tested the effects of LB on the development of fear learning and neuronal structures involved in emotional regulation, the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA). LB delayed the ability of peri-weanling (21 days old) mice to express, but not form, an auditory conditioned fear memory. LB accelerated the developmental emergence of parvalbumin (PV)-positive cells in the BLA and increased anatomical connections between PL and BLA. Fear expression in LB mice was rescued through optogenetic inactivation of PV-positive cells in the BLA. The current results provide a model of transiently blunted emotional reactivity in early development, with latent fear-associated memories emerging later in adolescence.

Inflammatory and Epigenetic Pathways for Perinatal Depression

2015 ◽  
Vol 18 (3) ◽  
pp. 331-343 ◽  
Author(s):  
Lindsey Garfield ◽  
Herbert L. Mathews ◽  
Linda Witek Janusek
Keyword(s):  
Early Life ◽  
Infant Health ◽  
Perinatal Depression ◽  
Life Experiences ◽  
Perinatal Period ◽  
Early Life Adversity ◽  
Targeted Interventions ◽  
Increased Risk ◽  
History Of ◽  
The Impact

Depression during the perinatal period is common and can have adverse consequences for women and their children. Yet, the biobehavioral mechanisms underlying perinatal depression are not known. Adverse early life experiences increase the risk for adult depression. One potential mechanism by which this increased risk occurs is epigenetic embedding of inflammatory pathways. The purpose of this article is to propose a conceptual model that explicates the linkage between early life adversity and the risk for maternal depression. The model posits that early life adversity embeds a proinflammatory epigenetic signature (altered DNA methylation) that predisposes vulnerable women to depression during pregnancy and the postpartum period. As proposed, women with a history of early life adversity are more likely to exhibit higher levels of proinflammatory cytokines and lower levels of oxytocin in response to the demands of pregnancy and new motherhood, both of which are associated with the risk for perinatal depression. The model is designed to guide investigations into the biobehavioral basis for perinatal depression, with emphasis upon the impact of early life adversity. Testing this model will provide a better understanding of maternal depressive risk and improve identification of vulnerable women who would benefit from targeted interventions that can reduce the impact of perinatal depression on maternal–infant health.

scholarly journals Early life adversity, dispositional mindfulness, and longitudinal stress experience during the COVID-19 pandemic

2020 ◽  
Author(s):  
Annika Benz ◽  
Maria Meier ◽  
Ulrike U. Bentele ◽  
Stephanie J. Dimitroff ◽  
Bernadette Denk ◽  
...  
Keyword(s):  
Perceived Stress ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Dispositional Mindfulness ◽  
Early Life Adversity ◽  
Stress Buffering ◽  
Psychopathological Symptoms ◽  
Increased Risk ◽  
The Impact

Experiencing severe or prolonged stressors in early life is associated with increased risk for mental and physical disorders in adulthood. Further, individuals who experienced early life stress (ELS) may use dysfunctional coping strategies like stress-related eating, in contrast to more beneficial stress buffering mechanisms e.g. based on mindfulness. Whether these mechanisms contribute to increased levels of perceived stress and symptoms of mental disorders in individuals with ELS in times of crisis is yet unclear. As part of a larger project, we assessed changes in perceived stress and psychopathological symptoms in a sample of N=102 participants (81% female; meanage=23.49, SDage= 7.11, range 18–62) from October/December 2019 (prior to the Covid-19 pandemic) to April/June 2020 (after the German government introduced Covid-19 related restrictions). Additionally, we assessed ELS and dispositional mindfulness.Perceived stress and depression significantly increased while anxiety levels decreased. No significant change was observed for somatization. ELS and dispositional mindfulness were not associated with change scores, but with perceived stress and psychopathological symptoms at both assessments. The increase in perceived stress during the pandemic in a majority of participants demonstrates the impact of the pandemic in the general population.

scholarly journals Parental socioeconomic position and chronic inflammation during adolescence

2019 ◽  
Vol 29 (Supplement_4) ◽  
Author(s):  
S Fraga ◽  
M Severo ◽  
E Ramos ◽  
M Kelly-Irving ◽  
S Silva ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Socioeconomic Position ◽  
Early Life ◽  
High Sensitivity ◽  
Early Life Adversity ◽  
Socioeconomic Environment ◽  
Reactive Protein ◽  
Increased Risk ◽  
Health Related ◽  
Inflammatory Processes

Abstract Background Early life adversity has been associated with increased risk of inflammation and inflammation-related diseases in adulthood. This study aimed to examine the association of parental socioeconomic position with chronic inflammation over adolescence. Methods We used information on 2942 members (1507 girls and 1435 boys) of the EPITeen cohort that was established in 2003 in Porto, Portugal, and included 13 years old adolescents that were further evaluated at 17 and 21 years. Mother’ and father’s education and occupation were used as indicators of parental socioeconomic position. High-sensitivity C-reactive protein (CRP) was measured at three points in time (13, 17 and 21 years). CRP levels were categorized in tertiles separately for each wave; chronic inflammation in adolescence was defined as having CRP levels in the highest tertile in at least 2 waves and never in the lowest tertile. Results Over adolescence, the prevalence of chronic inflammation was significantly higher among participants with low parental socioeconomic position. Low parental socioeconomic position was associated with chronic inflammation in adolescence, after adjustment for sex, perinatal and physical environment factors, health-related behaviours and health status in adolescence OR = 1.63; 95%CI: 1.11, 2.40 for lowest vs. highest mother’s education and OR = 1.61; 95%CI: 1.12, 2.30 for lowest vs. highest father’s education. Conclusions Low parental socioeconomic position is associated with chronic inflammation during adolescence. Our results suggest that the early life socioeconomic environment has an impact on inflammatory processes over adolescence.

scholarly journals Nutritional adversity, sex and reproduction: 30 years of DOHaD and what have we learned?

2019 ◽  
Vol 242 (1) ◽  
pp. T51-T68 ◽  
Author(s):  
Patrycja A Jazwiec ◽  
Deborah M Sloboda
Keyword(s):  
Germ Cells ◽  
Early Life ◽  
Disease Risk ◽  
Primordial Germ Cells ◽  
Reproductive Function ◽  
Postnatal Life ◽  
Early Life Adversity ◽  
Increased Risk ◽  
Health And Disease

It is well established that early life environmental signals, including nutrition, set the stage for long-term health and disease risk – effects that span multiple generations. This relationship begins early, in the periconceptional period and extends into embryonic, fetal and early infant phases of life. Now known as the Developmental Origins of Health and Disease (DOHaD), this concept describes the adaptations that a developing organism makes in response to early life cues, resulting in adjustments in homeostatic systems that may prove maladaptive in postnatal life, leading to an increased risk of chronic disease and/or the inheritance of risk factors across generations. Reproductive maturation and function is similarly influenced by early life events. This should not be surprising, since primordial germ cells are established early in life and thus vulnerable to early life adversity. A multitude of ‘modifying’ cues inducing developmental adaptations have been identified that result in changes in reproductive development and impairments in reproductive function. Many types of nutritional challenges including caloric restriction, macronutrient excess and micronutrient insufficiencies have been shown to induce early life adaptations that produce long-term reproductive dysfunction. Many pathways have been suggested to underpin these associations, including epigenetic reprogramming of germ cells. While the mechanisms still remain to be fully investigated, it is clear that a lifecourse approach to understanding lifetime reproductive function is necessary. Furthermore, investigations of the impacts of early life adversity must be extended to include the paternal environment, especially in epidemiological and clinical studies of offspring reproductive function.

scholarly journals Early Life Trauma Has Lifelong Consequences for Sleep And Behavior

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Monica Lewin ◽  
Jenna Lopachin ◽  
James Delorme ◽  
Maya Opendak ◽  
Regina M. Sullivan ◽  
...  
Keyword(s):  
Adverse Events ◽  
Sleep Quality ◽  
Emotional Regulation ◽  
Early Life ◽  
Sleep Problems ◽  
Later Life ◽  
Nrem Sleep ◽  
Early Life Adversity ◽  
Sleep Physiology ◽  
And Behavior

Abstract Sleep quality varies widely across individuals, especially during normal aging, with impaired sleep contributing to deficits in cognition and emotional regulation. Sleep can also be impacted by a variety of adverse events, including childhood adversity. Here we examined how early life adverse events impacted later life sleep structure and physiology using an animal model to test the relationship between early life adversity and sleep quality across the life span. Rat pups were exposed to an Adversity-Scarcity model from postnatal day 8–12, where insufficient bedding for nest building induces maternal maltreatment of pups. Polysomnography and sleep physiology were assessed in weaning, early adult and older adults. Early life adversity induced age-dependent disruptions in sleep and behavior, including lifelong spindle decreases and later life NREM sleep fragmentation. Given the importance of sleep in cognitive and emotional functions, these results highlight an important factor driving variation in sleep, cognition and emotion throughout the lifespan that suggest age-appropriate and trauma informed treatment of sleep problems.

The impact of early life gut colonization on metabolic and obesogenic outcomes: what have animal models shown us?

2015 ◽  
Vol 7 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J. G. Wallace ◽  
W. Gohir ◽  
D. M. Sloboda
Keyword(s):  
Animal Models ◽  
Gut Microbiota ◽  
Early Life ◽  
Maternal Obesity ◽  
Communicable Disease ◽  
Critical Periods ◽  
Early Life Adversity ◽  
Gut Colonization ◽  
Increased Risk ◽  
The Impact

The rise in the occurrence of obesity to epidemic proportions has made it a global concern. Great difficulty has been experienced in efforts to control this growing problem with lifestyle interventions. Thus, attention has been directed to understanding the events of one of the most critical periods of development, perinatal life. Early life adversity driven by maternal obesity has been associated with an increased risk of metabolic disease and obesity in the offspring later in life. Although a mechanistic link explaining the relationship between maternal and offspring obesity is still under investigation, the gut microbiota has come forth as a new factor that may play a role modulating metabolic function of both the mother and the offspring. Emerging evidence suggests that the gut microbiota plays a much larger role in mediating the risk of developing non-communicable disease, including obesity and metabolic dysfunction in adulthood. With the observation that the early life colonization of the neonatal and postnatal gut is mediated by the perinatal environment, the number of studies investigating early life gut microbial establishment continues to grow. This paper will review early life gut colonization in experimental animal models, concentrating on the role of the early life environment in offspring gut colonization and the ability of the gut microbiota to dictate risk of disease later in life.

scholarly journals Altered corticolimbic connectivity reveals sex-specific adolescent outcomes in a rat model of early life adversity

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jennifer A Honeycutt ◽  
Camila Demaestri ◽  
Shayna Peterzell ◽  
Marisa M Silveri ◽  
Xuezhu Cai ◽  
...  
Keyword(s):  
Early Life ◽  
Basolateral Amygdala ◽  
Maternal Separation ◽  
Female Rats ◽  
Resting State Functional Connectivity ◽  
Early Life Adversity ◽  
Adolescent Outcomes ◽  
Male And Female Rats ◽  
Neurobiological Substrates ◽  
Separate Cohort

Exposure to early-life adversity (ELA) increases the risk for psychopathologies associated with amygdala-prefrontal cortex (PFC) circuits. While sex differences in vulnerability have been identified with a clear need for individualized intervention strategies, the neurobiological substrates of ELA-attributable differences remain unknown due to a paucity of translational investigations taking both development and sex into account. Male and female rats exposed to maternal separation ELA were analyzed with anterograde tracing from basolateral amygdala (BLA) to PFC to identify sex-specific innervation trajectories through juvenility (PD28) and adolescence (PD38;PD48). Resting-state functional connectivity (rsFC) was assessed longitudinally (PD28;PD48) in a separate cohort. All measures were related to anxiety-like behavior. ELA-exposed rats showed precocial maturation of BLA-PFC innervation, with females affected earlier than males. ELA also disrupted maturation of female rsFC, with enduring relationships between rsFC and anxiety-like behavior. This study is the first providing both anatomical and functional evidence for sex- and experience-dependent corticolimbic development.

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