scholarly journals Social hierarchy position in female mice is associated with plasma corticosterone levels and hypothalamic gene expression

2019 ◽  
Author(s):  
Cait M. Williamson ◽  
Won Lee ◽  
Alexandra R. Decasien ◽  
Alesi Lanham ◽  
Russell D. Romeo ◽  
...  

AbstractSocial hierarchies emerge when animals compete for access to resources such as food, mates or physical space. Wild and laboratory male mice have been shown to develop linear hierarchies, however, less is known regarding whether female mice have sufficient intrasexual competition to establish significant social dominance relationships. In this study, we examined whether groups of outbred CD-1 virgin female mice housed in a large vivaria formed social hierarchies. We show that females use fighting, chasing and mounting behaviors to rapidly establish highly directionally consistent social relationships. Notably, these female hierarchies are less linear, steep and despotic compared to male hierarchies. Female estrus state was not found to have a significant effect on aggressive behavior, though dominant females had elongated estrus cycles (due to increased time in estrus) compared to subordinate females. Plasma estradiol levels were equivalent between dominant and subordinate females. Subordinate females had significantly lower levels of basal corticosterone compared to dominant females. Analyses of gene expression in the ventromedial hypothalamus indicated that subordinate females have elevated ERα, ERβ and OTR mRNA compared to dominant females. This study provides a methodological framework for the study of the neuroendocrine basis of female social aggression and dominance in laboratory mice.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Cait M. Williamson ◽  
Won Lee ◽  
Alexandra R. DeCasien ◽  
Alesi Lanham ◽  
Russell D. Romeo ◽  
...  

2021 ◽  
Author(s):  
Christopher H. Seward ◽  
Michael C Saul ◽  
Joseph M. Troy ◽  
Huimin Zhang ◽  
Lisa J Stubbs

In many species, adults will care for young offspring that are not their own, a phenomenon called alloparenting. However, most nonparental adults experience an initial aversion to newborns, which must be overcome before a robust display of parental-like behaviors can begin. To capture neurogenomic events underlying this dramatic behavioral transition, we analyzed brain gene expression and chromatin profiles of virgin female mice co-housed with mothers during pregnancy and after birth. After an initial display of agonistic behaviors and a surge of defense-related gene expression, we observed a dramatic shift in the chromatin landscape specifically in amygdala, accompanied by a dampening of the defense-related genes. This shift coincided with the emergence of behaviors and gene expression classically associated with maternal care. The results reveal the outlines of a neurogenomic program associated with this dramatic aversive-to-affiliative behavioral switch, and suggest molecular networks that may be relevant to human postpartum mental health.


Endocrinology ◽  
2014 ◽  
Vol 155 (9) ◽  
pp. 3674-3683 ◽  
Author(s):  
Danielle S. Stolzenberg ◽  
Jacqueline S. Stevens ◽  
Emilie F. Rissman

Abstract In many species, including mice, maternal responsiveness is experience-dependent and permanent, lasting for long periods (months to years). We have shown that after brief exposures to pups, virgin female mice continue to respond maternally toward pups for at least one month. Administration of a histone deacetylase inhibitor (HDACi) reduces the amount of maternal experience required to affect maternal behavior and gene expression. In this set of studies, we examined the epigenetic mechanisms that underlie these motivated behaviors. We assessed whether the effects of HDACi persisted 1 month after the initial experience (in the absence of continued pup experience or HDACi treatment) and whether the maintenance of maternal memory was associated with stable changes in gene expression. Using chromatin immunoprecipitation, we examined whether Esr2 and Oxt gene expression might be mediated by recruitment of the histone acetyltransferase cAMP response element binding protein (CBP) to their promoter regions after maternal memory consolidation. We report that HDACi treatment induced long-lasting changes in maternal responsiveness. Maternal learning was associated with increased recruitment of CBP to the Esr2 and Oxt gene promoters during the consolidation of maternal memory as well as a persistent increase in estrogen receptor-β (Esr2) mRNA and decreased expression of the de novo DNA methyltransferase Dnmt3a within the medial preoptic area. The consolidation of the maternal experience may involve the CBP recruitment and stable changes in gene expression, which maintain increased maternal responsiveness for long periods of time.


2020 ◽  
Vol 98 (11) ◽  
Author(s):  
Chao Yan ◽  
Kate Hartcher ◽  
Wen Liu ◽  
Jinlong Xiao ◽  
Hai Xiang ◽  
...  

Abstract Conditions in early life play profound and long-lasting effects on the welfare and adaptability to stress of chickens. This study aimed to explore the hypothesis that the provision of environmental complexity in early life improves birds’ adaptive plasticity and ability to cope with a challenge later in life. It also tried to investigate the effect of the gut-brain axis by measuring behavior, stress hormone, gene expression, and gut microbiota. One-day-old chicks were split into 3 groups: (1) a barren environment (without enrichment items) group (BG, n = 40), (2) a litter materials group (LG, n = 40), and (3) a perches with litter materials group (PLG, n = 40). Then, enrichment items were removed and simulated as an environmental challenge at 31 to 53 d of age. Birds were subjected to a predator test at 42 d of age. In the environmental challenge, when compared with LG, PLG birds were characterized by decreased fearfulness, lower plasma corticosterone, improved gut microbial functions, lower relative mRNA expression of GR, and elevated mRNA expressions of stress-related genes CRH, BDNF, and NR2A in the hypothalamus (all P < 0.05). Unexpectedly, the opposite was true for the LG birds when compared with the BG (P < 0.05). Decreased plasma corticosterone and fearfulness were accompanied by altered hypothalamic gene mRNA expressions of BDNF, NR2A, GR, and CRH through the HPA axis in response to altered gut microbial compositions and functions. The findings suggest that gut microbiota may integrate fearfulness, plasma corticosterone, and gene expression in the hypothalamus to provide an insight into the gut-brain axis in chicks. In conclusion, having access to both perches and litter materials in early life allowed birds to cope better with a future challenge. Birds in perches and litter materials environment may have optimal development and adaptive plasticity through the gut-brain axis.


2020 ◽  
pp. 194-228
Author(s):  
Michael Numan

Chapter 7 examines alloparental and paternal behavior. Although these behaviors are rare in mammals, their occurrence indicates that parental behavior can occur in the absence of pregnancy and parturition. For mammals of both sexes, dual brain circuits affect whether parental behavior occurs: An inhibitory defensive circuit (anterior hypothalamus/ventromedial hypothalamus projections to periaqueductal gray), and an excitatory parental circuit (medial preoptic area, mesolimbic dopamine system, and the oxytocin system). When alloparental behavior occurs, either through experimental genetic selection (virgin female laboratory house mice) or through natural selection (prairie voles, marmosets), the defensive circuit has been downregulated and the parental circuit has been upregulated by such selection. When paternal behavior occurs, either naturally (California mice, dwarf hamsters) or experimentally (laboratory rats and house mice), copulation with a female and remaining with her through parturition depresses the male’s defensive circuitry while activating his parental circuitry.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Saivageethi Nuthikattu ◽  
Dragan Milenkovic ◽  
John Rutledge ◽  
Amparo Villablanca

AbstractHyperlipidemia is a risk factor for dementia, and chronic consumption of a Western Diet (WD) is associated with cognitive impairment. However, the molecular mechanisms underlying the development of microvascular disease in the memory centers of the brain are poorly understood. This pilot study investigated the nutrigenomic pathways by which the WD regulates gene expression in hippocampal brain microvessels of female mice. Five-week-old female low-density lipoprotein receptor deficient (LDL-R−/−) and C57BL/6J wild type (WT) mice were fed a chow or WD for 8 weeks. Metabolics for lipids, glucose and insulin were determined. Differential gene expression, gene networks and pathways, transcription factors, and non-protein coding RNAs were evaluated by genome-wide microarray and bioinformatics analysis of laser captured hippocampal microvessels. The WD resulted in differential expression of 2,412 genes. The majority of differential gene expression was attributable to differential regulation of cell signaling proteins and their transcription factors, approximately 7% was attributable to differential expression of miRNAs, and a lesser proportion was due to other non-protein coding RNAs, primarily long non-coding RNAs (lncRNAs) and small nucleolar RNAs (snoRNAs) not previously described to be modified by the WD in females. Our findings revealed that chronic consumption of the WD resulted in integrated multilevel molecular regulation of the hippocampal microvasculature of female mice and may provide one of the mechanisms underlying vascular dementia.


1971 ◽  
Vol 45 (2-3) ◽  
pp. 223-228
Author(s):  
M. G. Taylor ◽  
D. A. Denham ◽  
G. S. Nelson

An attempt was made to demonstrate passive transfer of immunity using neonatal mice born to mothers resistant to schistosome infection. No immunity was demonstrated in the baby mice, suggesting that the classes of antibody which are active in this immune system are not transferrable neonatally.An interesting incidental finding was the apparent enhanced resistance of lactating mice compared to normal females or males and this was confirmed in another experiment. There was no significant difference between the susceptibility of normal females and male mice. More male worms were recovered from male mice than from virgin female mice.


1993 ◽  
Vol 265 (1) ◽  
pp. R117-R123
Author(s):  
Y. Matsui ◽  
H. Ishibashi ◽  
K. Kimura ◽  
M. Shiota ◽  
M. Ohta ◽  
...  

The responses of hepatic glycogenolysis to catecholamines in ventromedial hypothalamus (VMH)-lesioned male rats were examined in perfused livers. Seven days after bilateral electrical lesioning of the VMH, the livers were perfused. Isoproterenol, a beta-agonist, stimulated greater glucose production in VMH-lesioned rats than in controls (32.8 vs. 5.6 mumol glucose.h-1.g liver-1), while responses to phenylephrine, an alpha-agonist, decreased significantly compared with controls (44.4 vs. 69.8 mumol glucose.h-1.g liver-1). There were no significant differences in responses of livers to glucagon and vasopressin between control and VMH-lesioned rats. Adrenodemedullation showed the same effect on beta-responses as lesions in the VMH, but no effect on alpha-responses. Plasma epinephrine levels were not detectable with the high-performance liquid chromatography analysis in VMH-lesioned rats. The periodicity of plasma corticosterone levels was observed in both VMH-lesioned and control rats, although daytime increases in plasma corticosterone were blocked by VMH lesions. These results suggest that the lesions in the VMH cause changes in the levels of adrenergic receptor and that the increase in beta-responses is caused mostly by the reduction of plasma epinephrine.


Author(s):  
Luma Melo ◽  
Karen Tilmant ◽  
Amit Hagar ◽  
JAMES E KLAUNIG

Chronic endurance exercise is a therapeutic strategy in the treatment of many chronic diseases in humans, including the prevention and treatment of metabolic diseases such as diabetes mellitus. Metabolic, cardiorespiratory and endocrine pathways targeted by chronic endurance exercise have been identified. In the liver however, the cellular and molecular pathways that are modified by exercise and have preventive or therapeutic relevance to metabolic disease remain unresolved. The mouse model used in the current study allows for the quantification of a human-relevant exercise “dosage”. In this study we show hepatic gene expression differences between sedentary female and sedentary male mice, and that chronic exercise modifies the transcription of hepatic genes related to metabolic disease and steatosis in both male and female mice. Chronic exercise induces molecular pathways involved in glucose tolerance, glycolysis and gluconeogenesis while producing a decrease in pathways related to insulin resistance, steatosis, fibrosis, and inflammation. Given these findings, this mouse exercise model has potential to dissect the cellular and molecular hepatic changes following chronic exercise with application to understanding the role that chronic exercise plays in preventing human diseases. Novelty Bullets: • Exercise modifies the hepatic gene expression and hepatic pathways related to metabolic disease in male and female mice. • Gender differences were seen in hepatic gene expression between sedentary and exercised mice. • The mouse exercise model used in this study allows for application and evaluation of exercise effects in human disease


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