scholarly journals Early life adversity in piglets induces long-term upregulation of the enteric cholinergic nervous system and heightened, sex-specific secretomotor neuron responses

2016 ◽  
Vol 28 (9) ◽  
pp. 1317-1329 ◽  
Author(s):  
J. E. Medland ◽  
C. S. Pohl ◽  
L. L. Edwards ◽  
S. Frandsen ◽  
K. Bagley ◽  
...  
Keyword(s):  
Nervous System ◽  
Early Life ◽  
Early Life Adversity

Long-term effects of early pain and injury

2021 ◽  
pp. 21-37
Author(s):  
Orla Moriarty ◽  
Suellen M. Walker
Keyword(s):  
Nervous System ◽  
Early Life ◽  
Tissue Injury ◽  
Afferent Input ◽  
Laboratory Studies ◽  
Long Term Effects ◽  
Nociceptive Pathways ◽  
Noxious Stimuli ◽  
Underlying Mechanisms

Nociceptive pathways are functional following birth, and acute responses to noxious stimuli have been documented from early in development in clinical and laboratory studies. The ability of noxious afferent input to alter the level of sensitivity of nociceptive pathways in the adult nervous system, with, for example, the development of central sensitization, is well established. However, the developing nervous system has additional susceptibilities to alterations in neural activity, and pain in early life may produce effects not seen following the same input at older ages. As a result, early tissue injury may lead to persistent changes in somatosensory processing and altered sensitivity to future noxious stimuli. Furthermore, there is increasing evidence that neonatal pain can result in long-term changes in cognitive and affective behavior. Effects of pain in early life are superimposed on a highly plastic developing system, and long-term outcomes vary depending on the type and severity of the injury, and on the evaluation methods used. Laboratory studies allow evaluation of different injuries, potential confounding factors, underlying mechanisms, and potential analgesic modulation.

scholarly journals Early-life adversity programs long-term cytokine and microglia expression within the HPA axis in female Japanese quail

2019 ◽  
Vol 222 (6) ◽  
pp. jeb187039 ◽  
Author(s):  
David J. Walker ◽  
Cédric Zimmer ◽  
Maria Larriva ◽  
Susan D. Healy ◽  
Karen A. Spencer
Keyword(s):  
Hpa Axis ◽  
Japanese Quail ◽  
Early Life ◽  
Early Life Adversity

scholarly journals Early maternal loss affects diurnal cortisol slopes in immature but not mature wild chimpanzees

2020 ◽  
Author(s):  
Cédric Girard-Buttoz ◽  
Patrick J. Tkaczynski ◽  
Liran Samuni ◽  
Pawel Fedurek ◽  
Cristina Gomes ◽  
...  
Keyword(s):  
Reproductive Success ◽  
Hpa Axis ◽  
Early Life ◽  
Urinary Cortisol ◽  
Maternal Loss ◽  
Early Life Adversity ◽  
Diurnal Cortisol ◽  
Animal Populations ◽  
Cortisol Levels

AbstractIn mammals, early life adversity negatively affects survival and reproductive success. A key causal mechanism is proposed by the biological embedding model which posits that adversity experienced early in life has deleterious consequences on individual physiology across the lifespan. In particular, early life adversity is expected to be a severe stressor leading to long-term alteration of the hypothalamic pituitary adrenal (HPA) axis activity. Here we tested this idea by assessing whether, as in humans, maternal loss had short and long-term impacts on orphan chimpanzee urinary cortisol levels and diurnal urinary cortisol slopes, as an indicator of the HPA axis functioning. We used 18 years of data on 50 immature and 28 mature male wild chimpanzees belonging to four communities in Taï National Park, Ivory Coast. Immature orphans who experienced early maternal loss had diurnal cortisol slopes characterised by higher early morning and late afternoon cortisol levels indicative of high activation of the HPA axis. Recently orphaned immatures had higher cortisol levels than other immatures, possibly reflecting social and nutritional stress. However, unlike in humans, we did not find significantly different cortisol profiles in orphan and non-orphan adult male chimpanzees. Our study highlights that long-term alteration of stress physiology related to early life adversity may not be viable in some wild animal populations and/or that chimpanzees, as humans, may have access to mechanisms that buffer this physiological stress, such as adoption. Our results suggest that biological embedding of altered HPA axis function is unlikely to be a mechanism contributing to the demonstrated long-term fitness consequences of maternal loss, such as reduced reproductive success, in wild long-lived mammals.

scholarly journals Early-Life Adversity Leaves Its Imprint on the Oral Microbiome for More Than 20 Years and Is Associated with Long-Term Immune Changes

2021 ◽  
Vol 22 (23) ◽  
pp. 12682
Author(s):  
Eleftheria G. Charalambous ◽  
Sophie B. Mériaux ◽  
Pauline Guebels ◽  
Claude P. Muller ◽  
Fleur A. D. Leenen ◽  
...  
Keyword(s):  
Early Life ◽  
Amplicon Sequencing ◽  
Oral Microbiome ◽  
Early Life Adversity ◽  
Early Environment ◽  
Health Trajectories ◽  
Adaptive Immune Cells ◽  
16S Amplicon Sequencing ◽  
Immune Changes

The early-life microbiome (ELM) interacts with the psychosocial environment, in particular during early-life adversity (ELA), defining life-long health trajectories. The ELM also plays a significant role in the maturation of the immune system. We hypothesised that, in this context, the resilience of the oral microbiomes, despite being composed of diverse and distinct communities, allows them to retain an imprint of the early environment. Using 16S amplicon sequencing on the EpiPath cohort, we demonstrate that ELA leaves an imprint on both the salivary and buccal oral microbiome 24 years after exposure to adversity. Furthermore, the changes in both communities were associated with increased activation, maturation, and senescence of both innate and adaptive immune cells, although the interaction was partly dependent on prior herpesviridae exposure and current smoking. Our data suggest the presence of multiple links between ELA, Immunosenescence, and cytotoxicity that occur through long-term changes in the microbiome.

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 Lifelong reductions of PKMζ in ventral hippocampus of nonhuman primates exposed to early-life adversity due to unpredictable maternal care

2021 ◽  
Vol 28 (9) ◽  
pp. 341-347
Author(s):  
Sasha L. Fulton ◽  
Changchi Hsieh ◽  
Tobias Atkin ◽  
Ryan Norris ◽  
Eric Schoenfeld ◽  
...  
Keyword(s):  
Maternal Care ◽  
Early Life ◽  
Long Term Potentiation ◽  
Emotional Memory ◽  
Ventral Hippocampus ◽  
Long Term Memory ◽  
Early Life Adversity ◽  
Protein Kinase Mζ ◽  
Maternal Variable

Protein kinase Mζ (PKMζ) maintains long-term potentiation (LTP) and long-term memory through persistent increases in kinase expression. Early-life adversity is a precursor to adult mood and anxiety disorders, in part, through persistent disruption of emotional memory throughout life. Here we subjected 10- to 16-wk-old male bonnet macaques to adversity by a maternal variable-foraging demand paradigm. We then examined PKMζ expression in their ventral hippocampi as 7- to 12-yr-old adults. Quantitative immunohistochemistry reveals decreased PKMζ in dentate gyrus, CA1, and subiculum of subjects who had experienced early-life adversity due to the unpredictability of maternal care. Adult animals with persistent decrements of PKMζ in ventral hippocampus express timid rather than confrontational responses to a human intruder. Persistent down-regulation of PKMζ in the ventral hippocampus might reduce the capacity for emotional memory maintenance and contribute to the long-lasting emotional effects of early-life adversity.

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