Animal models of depression: Long-term neurobehavioral effects of early life adversity in rats and monkeys

2004 ◽  
Author(s):  
J. Feldon ◽  
D. Rueedi-Bettschen ◽  
H. Russig ◽  
A. C. Dettling ◽  
C. R. Pryce
2019 ◽  
Vol 222 (6) ◽  
pp. jeb187039 ◽  
Author(s):  
David J. Walker ◽  
Cédric Zimmer ◽  
Maria Larriva ◽  
Susan D. Healy ◽  
Karen A. Spencer

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

2020 ◽  
Author(s):  
Cédric Girard-Buttoz ◽  
Patrick J. Tkaczynski ◽  
Liran Samuni ◽  
Pawel Fedurek ◽  
Cristina Gomes ◽  
...  

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.


2020 ◽  
Author(s):  
Jamie Lars Hanson ◽  
Brendon Nacewicz

Early life adversity (ELA), such as child maltreatment or child poverty, engenders problems with emotional and behavioral regulation. In the quest to understand the neurobiological sequelae and mechanisms of risk, the amygdala has been of major focus. While the basic functions of this region make it a strong candidate for understanding the multiple mental health issues common after ELA, extant literature is marked by profound inconsistencies, with reports of larger, smaller, and no differences in regional volumes of this area. We believe integrative models of stress neurodevelopment, grounded in “allostatic load”, will help resolve inconsistencies in the impact of ELA on the amygdala. In this review, we attempt to connect past research studies to new findings with animal models of cellular and neurotransmitter mediators of stress buffering to extreme fear generalization onto testable research and clinical concepts. Drawing on the greater impact of inescapability over unpredictability in animal models, we propose a mechanism by which ELA aggravates an exhaustive cycle of amygdala expansion and subsequent toxic-metabolic damage. We connect this neurobiological sequela to psychosocial mal/adaptation after ELA, bridging to behavioral studies of attachment, emotion processing, and social functioning. Lastly, we conclude this review by proposing a multitude of future directions in preclinical work and studies of humans that suffered ELA.


2005 ◽  
Vol 29 (4-5) ◽  
pp. 649-674 ◽  
Author(s):  
Christopher R. Pryce ◽  
Daniela Rüedi-Bettschen ◽  
Andrea C. Dettling ◽  
Anna Weston ◽  
Holger Russig ◽  
...  

2010 ◽  
Vol 214 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Mathias V. Schmidt ◽  
Xiao-Dong Wang ◽  
Onno C. Meijer

2021 ◽  
Vol 22 (23) ◽  
pp. 12682
Author(s):  
Eleftheria G. Charalambous ◽  
Sophie B. Mériaux ◽  
Pauline Guebels ◽  
Claude P. Muller ◽  
Fleur A. D. Leenen ◽  
...  

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.


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