scholarly journals The influence of stress hormones and aggression on cooperative behaviour in subordinate meerkats

2017 ◽  
Vol 284 (1863) ◽  
pp. 20171248 ◽  
Author(s):  
Ben Dantzer ◽  
Ines Braga Goncalves ◽  
Helen C. Spence-Jones ◽  
Nigel C. Bennett ◽  
Michael Heistermann ◽  
...  

In cooperative breeders, aggression from dominant breeders directed at subordinates may raise subordinate stress hormone (glucocorticoid) concentrations. This may benefit dominants by suppressing subordinate reproduction but it is uncertain whether aggression from dominants can elevate subordinate cooperative behaviour, or how resulting changes in subordinate glucocorticoid concentrations affect their cooperative behaviour. We show here that the effects of manipulating glucocorticoid concentrations in wild meerkats ( Suricata suricatta ) on cooperative behaviour varied between cooperative activities as well as between the sexes. Subordinates of both sexes treated with a glucocorticoid receptor antagonist (mifepristone) exhibited significantly more pup protection behaviour (babysitting) compared to those treated with glucocorticoids (cortisol) or controls. Females treated with mifepristone had a higher probability of exhibiting pup food provisioning (pup-feeding) compared to those treated with cortisol. In males, there were no treatment effects on the probability of pup-feeding, but those treated with cortisol gave a higher proportion of the food they found to pups than those treated with mifepristone. Using 19 years of behavioural data, we also show that dominant females did not increase the frequency with which they directed aggression at subordinates at times when the need for assistance was highest. Our results suggest that it is unlikely that dominant females manipulate the cooperative behaviour of subordinates through the effects of aggression on their glucocorticoid levels and that the function of aggression directed at subordinates is probably to reduce the probability they will breed.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vitor Bonetti Valente ◽  
Diovana de Melo Cardoso ◽  
Giseli Mitsuy Kayahara ◽  
Giovana Barros Nunes ◽  
Kellen Cristine Tjioe ◽  
...  

AbstractChronic stress increases the systemic levels of stress hormones norepinephrine and cortisol. As well as tobacco-specific carcinogen NNK (4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone), they can induce expressive DNA damage contributing to the cancer development. However, it is unknown whether stress hormones have genotoxic effects in oral keratinocytes. This study investigated the effects of stress hormones on DNA damage in a human oral keratinocyte cell line (NOK-SI). NOK-SI cells stimulated with norepinephrine or cortisol showed higher DNA damage compared to untreated cells. Norepinephrine-induced DNA damage was reversed by pre-treatment with beta-adrenergic blocker propranolol. Cells treated with NNK combined to norepinephrine displayed reduced levels of caspases 3 and 7. Cortisol also reduced the activity of pro-apoptotic enzymes. NNK or norepinephrine promoted single-strand breaks and alkali-label side breaks in the DNA of NOK-SI cells. Pre-treatment of cells with propranolol abolished these effects. Carcinogen NNK in the presence or absence of cortisol also induced DNA damage of these cells. The genotoxic effects of cortisol alone and hormone combined with NNK were blocked partially and totally, respectively, by the glucocorticoid receptor antagonist RU486. DNA damage promoted by NNK or cortisol and carcinogen combined to the hormone led to intracellular γH2AX accumulation. The effects caused by NNK and cortisol were reversed by propranolol and glucocorticoid receptor antagonist RU486, respectively. Propranolol inhibited the oxidation of basis induced by NNK in the presence of DNA-formamidopyrimidine glycosylase. DNA breaks induced by norepinephrine in the presence or absence of NNK resulted in higher 8OHdG cellular levels. This effect was also induced through beta-adrenergic receptors. Together, these findings indicate that stress hormones induce DNA damage of oral keratinocytes and could contribute to oral carcinogenesis.


2019 ◽  
Vol 122 (6) ◽  
pp. 2636-2642
Author(s):  
Hui Li ◽  
Amanda J. Page

Gastric vagal afferent (GVA) sensing of food-related mechanical stimuli is a crucial mechanism in the control of feeding behavior and gastric function. Stress is an important factor contributing to eating disorders and gastric diseases. Chronic stress has been shown to increase the mechanosensitivity of GVAs in mice and to reduce food intake and body weight. Whether the mechanosensitivity of GVAs is modulated by stress hormones is not known. This study aimed to determine the effect of stress hormones on GVA mechanosensitivity. The expression of stress hormone receptors in GVA cell bodies was determined in 8-wk-old male C57BL/6 mice using quantitative RT-PCR combined with laser capture microdissection. The mechanosensitivity of GVAs was determined in the absence and presence of stress hormones using an in vitro single-fiber recording preparation. NR3C1 and CRHR2 (mRNA isoforms of glucocorticoid receptor and CRF2 receptor, respectively) were expressed in GVA neurons. The glucocorticoid receptor agonist corticosterone had no effect on the mechanosensitivity of either tension or mucosal GVAs. Activation of CRF2 receptor by its specific analog, urocortin 3, significantly increased the mechanosensitivity of both tension and mucosal GVAs, an effect prevented by the CRF2 receptor antagonist astressin 2B. In conclusion, activation of CRF2 receptor increases the mechanosensitivity of GVAs. This may contribute to the stress- and CRF2 receptor-associated changes in feeding behavior and gastric function, possibly contributing to the hypersensitivity of GVAs in chronic stress conditions. NEW & NOTEWORTHY Gastric vagal afferents (GVAs) relay food-related signals to the central nervous system, where they are processed, eventually leading to modulation of food intake and gastric function. GVA signaling can be modulated by an array of hormones. Stress has been shown to induce GVA hypersensitivity. This study demonstrates that GVA neurons express subtypes of stress hormone receptors, specifically CRF2. Furthermore, activation of CRF2 receptor increases GVA mechanosensitivity, which could have implications for food intake and gastric function.


2019 ◽  
Author(s):  
Toshiro Seki ◽  
Atsushi Yasuda ◽  
Natsumi Kitajima ◽  
Masami Seki ◽  
Masayuki Oki ◽  
...  

2021 ◽  
Vol 13 (1) ◽  
pp. 7-19
Author(s):  
Kamile Geist ◽  
Peggy Zoccola ◽  
Nathan Andary ◽  
Eugene Geist ◽  
Godwin Dogbey ◽  
...  

Consistent, prolonged, and nurturing interactions of a primary caregiver with an infant is necessary for optimal development of the infant. Lowering parental stress can promote positive caregiver-infant social interaction behaviors. Studies show that when caregivers use rhythm-based music and movement strategies during interactions with their infants, non-verbal communication, mutual attunement, and self-reported stress levels improve. The purpose of this pilot study was to determine caregiver benefits (stress hormones and positive interaction behaviors) when learning rhythm-based music with movement strategies while interacting with their infant. This was achieved through randomization of caregiver/infant dyads to a treatment (instructional intervention) or control condition with no instruction. Significantly lower salivary cortisol levels and lower salivary cortisol/DHEA ratio values pre-post were observed for the treatment condition as compared to control. These findings suggest that learning and using rhythm-based music and movement interventions are promising for lowering stress in caregivers. The impact of the intervention with families at risk due to stress-related environmental factors should be further investigated. In addition, observing social emotional behaviors and stress hormone levels of the infant is suggested.


ChemInform ◽  
2013 ◽  
Vol 44 (4) ◽  
pp. no-no
Author(s):  
Kiran Shah ◽  
Dipam Patel ◽  
Pradip Jadav ◽  
Mubeen Sheikh ◽  
Kalapatapu V. V. M. Sairam ◽  
...  

2000 ◽  
Vol 278 (2) ◽  
pp. R367-R372 ◽  
Author(s):  
Mitsuhiro Denda ◽  
Toru Tsuchiya ◽  
Peter M. Elias ◽  
Kenneth R. Feingold

Recent studies have shown that psychological stress can influence cutaneous barrier function, suggesting that this form of stress could trigger or aggravate skin disease. In the present study, we demonstrate that transfer of hairless mice to a different cage delays barrier recovery rates. Pretreatment with a phenothiazine sedative, chlorpromazine, before transfer of animals restored the kinetics of barrier recovery toward normal, suggesting that psychological stress is the basis for this alteration in barrier homeostasis. To determine the mechanism linking psychological stress to altered barrier recovery, we first demonstrated that plasma corticosterone levels increase markedly after transfer of animals to new cages and that pretreatment with chlorpromazine blocks this increase. Second, we demonstrated that the systemic administration of corticosterone delays barrier recovery. Finally, we demonstrated that pretreatment with the glucocorticoid receptor antagonist RU-486 blocks the delay in barrier recovery produced by systemic corticosterone, change of cage, or immobilization. These results suggest that psychological stress stimulates increased production of glucocorticoids, which, in turn, adversely affects permeability barrier homeostasis.


2019 ◽  
Vol 3 ◽  
pp. 247028971986255
Author(s):  
Robert-Paul Juster

In this selective review, emerging literature linking biological sex, sociocultural gender, and sexual orientation to stress hormone functioning and multisystemic physiological dysregulations are summarized. Beyond sex as a binary biological variable, continuums of sex hormones, gender roles, gender identity, and sexual orientation each uniquely help delineate pathways and mechanisms linked to stress-related disease trajectories. This implicates glucocorticoid functioning and allostatic load, the “wear and tear” of chronic stress in synergy with unhealthy behaviors. Clinical considerations are also discussed for the field of gender medicine.


2019 ◽  
Vol 374 (1770) ◽  
pp. 20180117 ◽  
Author(s):  
Ben Dantzer ◽  
Constance Dubuc ◽  
Ines Braga Goncalves ◽  
Dominic L. Cram ◽  
Nigel C. Bennett ◽  
...  

The phenotype of parents can have long-lasting effects on the development of offspring as well as on their behaviour, physiology and morphology as adults. In some cases, these changes may increase offspring fitness but, in others, they can elevate parental fitness at a cost to the fitness of their offspring. We show that in Kalahari meerkats ( Suricata suricatta ), the circulating glucocorticoid (GC) hormones of pregnant females affect the growth and cooperative behaviour of their offspring. We performed a 3-year experiment in wild meerkats to test the hypothesis that GC-mediated maternal effects reduce the potential for offspring to reproduce directly and therefore cause them to exhibit more cooperative behaviour. Daughters (but not sons) born to mothers treated with cortisol during pregnancy grew more slowly early in life and exhibited significantly more of two types of cooperative behaviour (pup rearing and feeding) once they were adults compared to offspring from control mothers. They also had lower measures of GCs as they aged, which could explain the observed increases in cooperative behaviour. Because early life growth is a crucial determinant of fitness in female meerkats, our results indicate that GC-mediated maternal effects may reduce the fitness of offspring, but may elevate parental fitness as a consequence of increasing the cooperative behaviour of their daughters. This article is part of the theme issue ‘Developing differences: early-life effects and evolutionary medicine’.


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