Evolution of stress responses refine mechanisms of social rank
TL;DR: The evolution of social status appears to be inseparably connected to the evolution of stress as discussed by the authors, and it seems likely that the balance of regulatory elements in pro-and anti-stress neurocircuitries results in rapid but brief stress responses that are advantageous to social dominance.
About: This article is published in Neurobiology of Stress.The article was published on 2021-04-21 and is currently open access. It has received 4 citations till now. The article focuses on the topics: Aggression & Dominance (ethology).
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TL;DR: It is suggested that catecholamine concentrations in the forebrain of untreated responders are associated with chemical and visual communication in lizards and that signaler AVT alters this relationship for some, but not all, aspects of social communication.
Abstract: Dynamic fluctuations in the distribution of catecholamines across the brain modulate the responsiveness of vertebrates to social stimuli. Previous work demonstrates that green anoles (Anolis carolinensis) increase chemosensory behavior in response to males treated with exogenous arginine vasotocin (AVT), but the neurochemical mechanisms underlying this behavioral shift remains unclear. Since central catecholamine systems, including dopamine, rapidly activate in response to social stimuli, we tested whether exogenous AVT in signalers (stimulus animals) impacts catecholamine concentrations in the forebrain (where olfactory and visual information are integrated and processed) of untreated lizard responders. We also tested whether AVT influences the relationship between forebrain catecholamine concentrations and communication behavior in untreated receivers. We measured global catecholamine (dopamine = DA, epinephrine = Epi, and norepinephrine = NE) concentrations in the forebrain of untreated responders using high-performance liquid chromatography-mass spectrometry following either a 30-min social interaction with a stimulus male or a period of social isolation. Stimulus males were injected with exogenous AVT or vehicle saline (SAL). We found that global DA, but not Epi or NE, concentrations were elevated in lizards responding to SAL-males relative to isolated lizards. Lizards interacting with AVT-males had DA, Epi and NE concentrations that were not significantly different from SAL or isolated groups. For behavior, we found a significant effect of social treatment (AVT vs. SAL) on the relationships between (1) DA concentrations and the motivation to perform a chemical display (latency to tongue flick) and (2) Epi concentrations and time spent displaying mostly green body coloration. We also found a significant negative correlation between DA concentrations and the latency to perform a visual display but found no effect of social treatment on this relationship. These data suggest that catecholamine concentrations in the forebrain of untreated responders are associated with chemical and visual communication in lizards and that signaler AVT alters this relationship for some, but not all, aspects of social communication.
1 citations
TL;DR: It is suggested that insight into the mechanistic and evolutionary underpinnings of stress buffering in vertebrates can be gained from the study of social buffering of stress in fishes.
Abstract: Social buffering of stress refers to the effect of a social partner in reducing the cortisol or corticosterone response to a stressor. It has been well studied in mammals, particularly those that form pair bonds. Recent studies on fishes suggest that social buffering of stress also occurs in solitary species, gregarious species that form loose aggregations and species with well-defined social structures and bonds. The diversity of social contexts in which stress buffering has been observed in fishes holds promise to shed light on the evolution of this phenomenon among vertebrates. Equally, the relative simplicity of the fish brain is advantageous for identifying the neural mechanisms responsible for social buffering. In particular, fishes have a relatively small and simple forebrain but the brain regions that are key to social buffering, including the social behaviour network, the amygdala and the hypothalamic–pituitary–adrenal/interrenal axis, are functionally conserved across vertebrates. Thus, we suggest that insight into the mechanistic and evolutionary underpinnings of stress buffering in vertebrates can be gained from the study of social buffering of stress in fishes.
1 citations
1 citations
TL;DR: In this article , the authors explain how accelerated biological aging equates to slow phenoptosis, a phenomenon that occurs even in the prenatal stage and is theoretically supported by W. D. Hamilton's proposal that offsprings detecting they have dangerous mutations should then automatically speed their demise, in order to improve their fitness by giving their parents the chance to produce other fitter siblings.
Abstract: Vladimir Skulachev's coining of the term "phenoptosis" 25 years ago (Skulachev, V. P., Biochemistry (Moscow), 62, 1997) highlighted the theoretical possibility that aging is a programmed process to speed the exit of individuals posing some danger to their social group. While rapid "acute phenoptosis" might occur at any age (e.g., to prevent spread of deadly infections), "slow phenoptosis" is generally considered to occur later in life in the form of chronic age-related disorders. However, recent research indicates that risks for such chronic disorders can be greatly raised by early life adversity, especially during the prenatal stage. Much of this research uses indicators of biological aging, the speeding or slowing of natural physiological deterioration in response to environmental inputs, leading to divergence from chronological age. Studies using biological aging indicators commonly find it is accelerated not only in older individuals with chronic disorders, but also in very young individuals with health problems. This review will explain how accelerated biological aging equates to slow phenoptosis. Its occurrence even in the prenatal stage is theoretically supported by W. D. Hamilton's proposal that offsprings detecting they have dangerous mutations should then automatically speed their demise, in order to improve their inclusive fitness by giving their parents the chance to produce other fitter siblings.
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01 Jan 1956
TL;DR: In this paper, the discovery of stress, the dissection of stress the disease of adaptation sketch for a unified theory implications and applications is described, and the authors propose a unified framework for adaptation.
Abstract: The discovery of stress the dissection of stress the disease of adaptation sketch for a unified theory implications and applications.
5,551 citations
TL;DR: This paper summarizes the current views on coping styles as a useful concept in understanding individual adaptive capacity and vulnerability to stress-related disease and indicates the existence of a proactive and a reactive coping style in feral populations.
2,555 citations
TL;DR: The first evidence for collective memory is presented in such animal groups (where the previous history of group structure influences the collective behaviour exhibited as individual interactions change) during the transition of a group from one type of collective behaviour to another.
1,906 citations
TL;DR: The results suggest that amygdala damage is associated with impairment in decision-making and that the roles played by the amygdala and VMF in decision -making are different.
Abstract: The somatic marker hypothesis proposes that decision-making is a process that depends on emotion. Studies have shown that damage of the ventromedial prefrontal (VMF) cortex precludes the ability to use somatic (emotional) signals that are necessary for guiding decisions in the advantageous direction. However, given the role of the amygdala in emotional processing, we asked whether amygdala damage also would interfere with decision-making. Furthermore, we asked whether there might be a difference between the roles that the amygdala and VMF cortex play in decision-making. To address these two questions, we studied a group of patients with bilateral amygdala, but not VMF, damage and a group of patients with bilateral VMF, but not amygdala, damage. We used the "gambling task" to measure decision-making performance and electrodermal activity (skin conductance responses, SCR) as an index of somatic state activation. All patients, those with amygdala damage as well as those with VMF damage, were (1) impaired on the gambling task and (2) unable to develop anticipatory SCRs while they pondered risky choices. However, VMF patients were able to generate SCRs when they received a reward or a punishment (play money), whereas amygdala patients failed to do so. In a Pavlovian conditioning experiment the VMF patients acquired a conditioned SCR to visual stimuli paired with an aversive loud sound, whereas amygdala patients failed to do so. The results suggest that amygdala damage is associated with impairment in decision-making and that the roles played by the amygdala and VMF in decision-making are different.
1,892 citations
TL;DR: It is shown that viral-mediated, mesolimbic dopamine pathway–specific knockdown of brain-derived neurotrophic factor is required for the development of experience-dependent social aversion in mice experiencing repeated aggression.
Abstract: Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development of this experience-dependent social aversion. Gene profiling in the nucleus accumbens indicates that local knockdown of BDNF obliterates most of the effects of repeated aggression on gene expression within this circuit, with similar effects being produced by chronic treatment with antidepressant. These results establish an essential role for BDNF in mediating long-term neural and behavioral plasticity in response to aversive social experiences.
1,873 citations