scholarly journals Early-life social environment alters juvenile behavior and neuroendocrine function in a highly social cichlid fish

2018 ◽  
Author(s):  
Tessa K. Solomon-Lane ◽  
Hans A. Hofmann

AbstractEarly-life experiences can shape adult behavior, with consequences for fitness and health, yet fundamental questions remain unanswered about how early-life social experiences are translated into variation in brain and behavior. The African cichlid fish Astatotilapia burtoni, a model system in social neuroscience, is well known for its highly plastic social phenotypes in adulthood. Here, we rear juveniles in either social groups or pairs to investigate the effects of early-life social environments on behavior and neuroendocrine gene expression. We find that both juvenile behavior and neuroendocrine function are sensitive to early-life effects. Behavior robustly co-varies across multiple contexts (open field, social cue investigation, and dominance behavior assays) to form a behavioral syndrome, with pair-reared juveniles towards the end of syndrome that is less active and socially interactive. Pair-reared juveniles also submit more readily as subordinates. In a separate cohort, we measured whole brain expression of stress and sex hormone genes. Expression of glucocorticoid receptor (GR) 1a was elevated in group-reared juveniles, supporting a highly-conserved role for the stress axis mediating early-life effects. The effect of rearing environment on androgen receptor (AR) α and estrogen receptor (ER) α expression was mediated by treatment duration (1 vs. 5 weeks). Finally, expression of corticotropin-releasing factor (CRF) and GR2 decreased significantly over time. Rearing environment also caused striking differences in gene co-expression, such that expression was tightly integrated in pair-reared juveniles, but not group-reared or isolates. Together, this research demonstrates the important developmental origins of behavioral phenotypes and identifies potential behavioral and neuroendocrine mechanisms.

2015 ◽  
Vol 113 (3) ◽  
pp. 883-889 ◽  
Author(s):  
Jinghong Xu ◽  
Liping Yu ◽  
Terrence R. Stanford ◽  
Benjamin A. Rowland ◽  
Barry E. Stein

The brain's ability to integrate information from different senses is acquired only after extensive sensory experience. However, whether early life experience instantiates a general integrative capacity in multisensory neurons or one limited to the particular cross-modal stimulus combinations to which one has been exposed is not known. By selectively restricting either visual-nonvisual or auditory-nonauditory experience during the first few months of life, the present study found that trisensory neurons in cat superior colliculus (as well as their bisensory counterparts) became adapted to the cross-modal stimulus combinations specific to each rearing environment. Thus, even at maturity, trisensory neurons did not integrate all cross-modal stimulus combinations to which they were capable of responding, but only those that had been linked via experience to constitute a coherent spatiotemporal event. This selective maturational process determines which environmental events will become the most effective targets for superior colliculus-mediated shifts of attention and orientation.


2021 ◽  
Vol 75 (12) ◽  
Author(s):  
Aurélie Cohas ◽  
Coraline Bichet ◽  
Rébecca Garcia ◽  
Sylvia Pardonnet ◽  
Sophie Lardy ◽  
...  
Keyword(s):  

2013 ◽  
Vol 143 (1) ◽  
pp. 104-116 ◽  
Author(s):  
James A. Crossman ◽  
Kim T. Scribner ◽  
Christin A. Davis ◽  
Patrick S. Forsythe ◽  
Edward A. Baker

2016 ◽  
Vol 124 ◽  
pp. 82-90 ◽  
Author(s):  
Fernando J. Meijide ◽  
Graciela Rey Vázquez ◽  
Yanina G. Piazza ◽  
Paola A. Babay ◽  
Raúl F. Itria ◽  
...  

Endocrinology ◽  
2011 ◽  
Vol 152 (12) ◽  
pp. 4496-4503 ◽  
Author(s):  
Rachel Yehuda ◽  
Jonathan Seckl

Several stress-associated neuropsychiatric disorders, notably posttraumatic stress disorder and chronic pain and fatigue syndromes, paradoxically exhibit somewhat low plasma levels of the stress hormone cortisol. The effects appear greatest in those initially traumatized in early life, implying a degree of developmental programming, perhaps of both lower cortisol and vulnerability to psychopathology. In these conditions, lowered cortisol is not due to any adrenal or pituitary insufficiency. Instead, two processes appear involved. First, there is increased target cell sensitivity to glucocorticoid action, notably negative feedback upon the hypothalamic-pituitary-adrenal (stress) axis. Altered density of the glucocorticoid receptor is inferred, squaring with much preclinical data showing early life challenges can permanently program glucocorticoid receptors in a tissue-specific manner. These effects involve epigenetic mechanisms. Second, early life trauma/starvation induces long-lasting lowering of glucocorticoid catabolism, specifically by 5α-reductase type 1 (predominantly a liver enzyme) and 11β-hydroxysteroid dehydrogenase type 2 (in kidney), an effect also seen in model systems. These changes reflect a plausible early-life adaptation to increase the persistence of active cortisol in liver (to maximize fuel output) and kidney (to increase salt retention) without elevation of circulating levels, thus avoiding their deleterious effects on brain and muscle. Modestly lowered circulating cortisol and increased vulnerability to stress-associated disorders may be the outcome. This notion implies a vulnerable early-life phenotype may be discernable and indicates potential therapy by modest glucocorticoid replacement. Indeed, early clinical trials with cortisol have shown a modicum of promise.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 903-903
Author(s):  
Joanne Fil ◽  
Sangyun Joung ◽  
Courtney Hayes ◽  
Ryan N Dilger

Abstract Objectives Artificial rearing of pigs provides a number of advantages over conventional rearing (i.e., true maternal care), including careful control of nutrient intake and environment conditions. Yet there remains a gap in knowledge when comparing brain development between sow-reared and artificially-reared domestic pigs. Thus, our research sought to model brain development and assess recognition memory in a longitudinal manner by directly comparing rearing environments. Methods Forty-four intact (i.e., not castrated) male pigs were artificially-reared or sow-reared from postnatal day 2 until postnatal week 4. After postnatal week 4, all pigs were housed in a group setting within the same environment until postnatal week 24. Magnetic resonance imaging was conducted on pigs at 8 longitudinal time-points to model developmental trajectories of brain macrostrutural and microstructural outcomes. Additionally, pigs behavior were tested using the novel object recognition task at postnatal weeks 4 and 8. Results Throughout the 24-week study, no differences between rearing groups were noted in weekly body weights, average growth and feed intake patterns, or feed efficiency. Whole brain, grey matter, white matter, and cerebrospinal fluid growth patterns also did not differ between pigs assigned to different early-life rearing environments. Moreover, minimal differences in regional absolute volumes and fractional anisotropy developmental trajectories were identified, though artificially-reared pigs exhibited higher initial rates of myelination in multiple brain regions compared with sow-reared pigs. Furthermore, behavioral assessment at both PNW 4 and 8 suggested little influence of rearing environment on recognition memory, however, an age-dependent increase in object recognition memory was observed in the sow-reared group. Conclusions Our findings suggest that early-life rearing environment has little influence on brain growth trajectories and behavior in the domestic pig. Artificial rearing may promote maturation in certain brain areas but does not appear to elicit long-term effects in outcomes including brain structure or behavior. Funding Sources The study was funded by Société des Produits Nestlé SA.


2019 ◽  
Vol 374 (1785) ◽  
pp. 20190283 ◽  
Author(s):  
S. M. Géranton

Animal behaviours are affected not only by inherited genes but also by environmental experiences. For example, in both rats and humans, stressful early-life events such as being reared by an inattentive mother can leave a lasting trace and affect later stress response in adult life. This is owing to a chemical trace left on the chromatin attributed to so-called epigenetic mechanisms. Such an epigenetic trace often has consequences, sometimes long-lasting, on the functioning of our genes, thereby allowing individuals to rapidly adapt to a new environment. One gene under such epigenetic control is FKBP5 , the gene that encodes the protein FKPB51, a crucial regulator of the stress axis and a significant driver of chronic pain states. In this article, we will discuss the possibility that exposure to stress could drive the susceptibly to chronic pain via epigenetic modifications of genes within the stress axis such as FKBP5 . The possibility that such modifications, and therefore, the susceptibility to chronic pain, could be transmitted across generations in mammals and whether such mechanisms may be evolutionarily conserved across phyla will also be debated. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.


2019 ◽  
Vol 374 (1770) ◽  
pp. 20180119 ◽  
Author(s):  
Maria Reyes-Contreras ◽  
Gaétan Glauser ◽  
Diana J. Rennison ◽  
Barbara Taborsky

In many vertebrate species, early social experience generates long-term effects on later life social behaviour. These effects are accompanied by persistent modifications in the expression of genes implicated in the stress axis. It is unknown, however, whether stress axis programming can affect the development of social competence, and if so, by which mechanism(s). Here, we used pharmacological manipulations to persistently reprogramme the hypothalamic–pituitary–interrenal axis of juvenile cooperatively breeding cichlids, Neolamprologus pulcher. During the first two months of life, juveniles were repeatedly treated with cortisol, mifepristone or control treatments. Three months after the last manipulation, we tested for treatment effects on (i) social competence, (ii) the expression of genes coding for corticotropin-releasing factor ( crf ), glucocorticoid receptor ( gr1 ) and mineralocorticoid receptor ( mr ) in the telencephalon and hypothalamus and (iii) cortisol levels. Social competence in a social challenge was reduced in cortisol-treated juveniles, which is in accordance with previous work applying early-life manipulations using different social experiences. During early life, both cortisol and mifepristone treatments induced a persistent downregulation of crf and upregulation of mr in the telencephalon. We suggest that these persistent changes in stress gene expression may represent an effective physiological mechanism for coping with stress. This article is part of the theme issue ‘Developing differences: early-life effects and evolutionary medicine’.


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