Essential Role of Ovarian Hormones in Susceptibility to the Consequences of Witnessing Social Defeat in Female Rats

Finnell, Julie E.; Muniz, Brandon L.; Padi, Akhila; Lombard, Calliandra M.; Moffitt, Casey M.; Wood, Christopher S.; Wilson, L. Britt; Reagan, Lawrence P.; Wilson, Marlene A.; Wood, Susan K.

doi:10.1016/j.biopsych.2018.01.013

Cited by 54 publications

(67 citation statements)

References 102 publications

(118 reference statements)

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“…We have recently validated a new social stress model in females which effectively combines the olfactory, auditory, and visual stimulus of social defeat with a witness component. Using this model of witness stress, we were able to show that intact cycling females were more sensitive to the emergence of stress-induced depressive-like behaviors (Finnell et al, 2018). Moreover, these behaviors were associated with significant enhancements in neuroinflammation in the CeA (Finnell et al, 2018).…”

Section: Future Directionsmentioning

confidence: 89%

“…Women are not only more likely to develop depression and anxiety (Almeida, 2005;Feinstein et al, 2014;Nicodimos et al, 2009) but are also more sensitive to inflammatory related diseases (Kim et al, 2015). One of the major limitations in studying female stress sensitivity has been the inherent difficulty associated with using common social stress models, such as the social defeat paradigm described herein, with females (Finnell and Wood, 2018). We have recently validated a new social stress model in females which effectively combines the olfactory, auditory, and visual stimulus of social defeat with a witness component.…”

Section: Future Directionsmentioning

confidence: 99%

“…Notably, enhanced inflammation in the periphery and the brain has been reported to occur following repeated social stress exposure, producing enhanced cytokine concentrations in the plasma (Finnell et al, 2017a;Hodes et al, 2014;Powell et al, 2013;Wood et al, 2015) and distinct inflammatory profiles in the LC (Finnell et al, 2017a;Wood et al, 2015) and LC projection regions including the dorsal raphe (DR) (Finnell et al, 2017a;Wood et al, 2015) and central amygdala (CeA) (Finnell et al, 2018;Muhie et al, 2017). Several of these studies further identified that stress-induced proinflammatory cytokine release is causal to this depressive-like phenotype as administration of an IL-1 receptor antagonist (Wood et al, 2015), resveratrol (Finnell et al, 2017a), a natural polyphenol with potent anti-inflammatory actions, or bone marrow transplant to reduce IL-6 (Hodes et al, 2014) could block the emergence of stress-induced behavioral dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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The contribution of the locus coeruleus-norepinephrine system in the emergence of defeat-induced inflammatory priming

Finnell

Moffitt

Hesser

et al. 2019

Brain, Behavior, and Immunity

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Exposure to psychosocial stress is known to precipitate the emergence of stress related psychiatric disorders such as depression and anxiety. While mechanisms by which this occurs remain largely unclear, recent evidence points towards a causative role for inflammation. Neurotransmitters, such as norepinephrine (NE) are capable of regulating expression of proinflammatory cytokines and thus may contribute to the emergence of stress-related disorders. The locus coeruleus (LC) is the major source of norepinephrine (NE) to the brain and therefore the current study utilized N-(2chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), an LC selective noradrenergic neurotoxin, to determine the discrete involvement of the LC-NE system in social defeat-induced inflammation in LC projection regions including the central amygdala (CeA), dorsal raphe (DR) and plasma. In the current study, rats were exposed to brief social defeat or control manipulations on 5 consecutive days. To determine whether a history of social defeat enhanced or "primed" the inflammatory response to a subsequent defeat exposure, all rats regardless of stress history were exposed to an acute social defeat challenge immediately prior to tissue collection. As anticipated, prior history of social defeat primed inflammatory responses in the plasma and CeA while neuroinflammation in the DR was markedly reduced. Notably, DSP-4 treatment suppressed stress-induced circulating inflammatory cytokines independent of prior stress history. In contrast, neuroinflammation in the CeA and DR were greatly augmented selectively in DSP-4 treated rats with a history of social defeat. Together these data highlight the dichotomous nature of NE in stress-induced inflammatory priming in the periphery and the brain and directly implicate the LC-NE system in these processes.

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Section: Future Directionsmentioning

confidence: 89%

Section: Future Directionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The contribution of the locus coeruleus-norepinephrine system in the emergence of defeat-induced inflammatory priming

Finnell

Moffitt

Hesser

et al. 2019

Brain, Behavior, and Immunity

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“…With this in mind, a new model of social stress has recently emerged that combines the olfactory, auditory and visual exposure of social defeat without requiring the physical interaction of defeat. Using this vicarious witness stress model originally developed for use in male mice by Warren et al ( 2013 ), we have shown that intact female rats demonstrate greater sensitivity to the inflammatory, cardiovascular and behavioral consequences of witness stress exposure compared to ovariectomized female rats (Finnell et al, 2018 ). We have further demonstrated that this enhanced and prolonged behavioral and physiological sensitivity to the consequences of witness stress is not exhibited to the same extent in male rats (Finnell et al, 2017b ).…”

Section: Sources Of Individual Differences In Inflammatory Stress Resmentioning

confidence: 99%

“…However, preclinical and clinical studies have shown that there is considerable individual variability in the behavioral and inflammatory consequences induced by stress exposure resulting in the emergence of resilient and susceptible subpopulations. Specifically, it has been shown that greater inflammatory responses to stress are associated with greater negative affect in humans (Dickerson et al, 2009 ) and promote the development of depressive-like behaviors in rodents (Wohleb et al, 2013 , 2014a , b ; Hodes et al, 2014 ; Wood et al, 2015 ; Finnell and Wood, 2016 ; Finnell et al, 2017a , b , 2018 ). These stress-induced inflammatory effects are known to extend well beyond the immediate response to stress such that late phase inflammatory responses are also enhanced following social stress exposure (Kiecolt-Glaser et al, 2008 ; Deak et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress

Finnell

Wood

2018

Front. Behav. Neurosci.

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It has been well recognized that exposure to stress can lead to the onset of psychosocial disorders such as depression. While there are a number of antidepressant therapies currently available and despite producing immediate neurochemical alterations, they require weeks of continuous use in order to exhibit antidepressant efficacy. Moreover, up to 30% of patients do not respond to typical antidepressants, suggesting that our understanding of the pathophysiology underlying stress-induced depression is still limited. In recent years inflammation has become a major focus in the study of depression as several clinical and preclinical studies have demonstrated that peripheral and central inflammatory mediators, including interleukin (IL)-1β, are elevated in depressed patients. Moreover, it has been suggested that inflammation and particularly neuroinflammation may be a direct and immediate link in the emergence of stress-induced depression due to the broad neural and glial effects that are elicited by proinflammatory cytokines. Importantly, individual differences in inflammatory reactivity may further explain why certain individuals exhibit differing susceptibility to the consequences of stress. In this review article, we discuss sources of individual differences such as age, sex and coping mechanisms that are likely sources of distinct changes in stress-induced neuroimmune factors and highlight putative sources of exaggerated neuroinflammation in susceptible individuals. Furthermore, we review the current literature of specific neural and glial mechanisms that are regulated by stress and inflammation including mitochondrial function, oxidative stress and mechanisms of glutamate excitotoxicity. Taken together, the impetus for this review is to move towards a better understanding of mechanisms regulated by inflammatory cytokines and chemokines that are capable of contributing to the emergence of depressive-like behaviors in susceptible individuals.

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Emotional contagion in nonhuman animals: A review

Pérez-Manrique

Gomila

2021

WIRES Cognitive Science

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Emotional contagion, the emotional state‐matching of an individual with another, seems to be crucial for many social species. In recent years evidence on emotional contagion in different animal species has accumulated. However, despite its adaptative advantages and its presumed simplicity, the study and direct demonstration of this phenomenon present more complexities than previously thought. For these reasons, a review of the literature on emotional contagion in nonhuman species is timely to integrate current findings. In this paper thus, we carry out a comprehensive review of the most relevant studies on emotional contagion in animals and discuss the main problems and challenges of the field. We conclude that more research is needed to broaden our understanding of the mechanisms and functions of emotional contagion and the extent to which this process is present in a wide variety of species. Furthermore, the comparative study of emotional contagion would benefit from the use of systematized paradigms including both behavioral and physiological measures and the simultaneous recording of the responses of the interacting individuals to reliably assess an emotional state‐matching between them and reliable controls. This article is categorized under: Cognitive Biology > Evolutionary Roots of Cognition Psychology > Comparative Psychology Psychology > Emotion and Motivation

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Essential Role of Ovarian Hormones in Susceptibility to the Consequences of Witnessing Social Defeat in Female Rats

Abstract: Together these data suggest that ovarian hormones play a critical role in the behavioral, inflammatory, and cardiovascular susceptibility to social stress in female rats and reveal putative systems that are sensitized to stress in an ovarian hormone-dependent manner.

Cited by 54 publications

References 102 publications

The contribution of the locus coeruleus-norepinephrine system in the emergence of defeat-induced inflammatory priming

The contribution of the locus coeruleus-norepinephrine system in the emergence of defeat-induced inflammatory priming

Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress

Emotional contagion in nonhuman animals: A review

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