Social defeat protocol and relevant biomarkers, implications for stress response physiology, drug abuse, mood disorders and individual stress vulnerability: a systematic review of the last decade

Vasconcelos, Mailton; Stein, Dirson João; Almeida, Rosa M. M. de

doi:10.1590/2237-6089-2014-0034

Cited by 51 publications

(23 citation statements)

References 123 publications

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“…Brain‐derived neurotrophic factor (BDNF) is strongly linked to the mesolimbic pathway, promoting the release of DA through activation of tropomyosin receptor kinase B (TrkB), and there is interaction among neural mechanisms in response to cocaine or stress affecting DA and BDNF (Goggi, Pullar, Carney, & Bradford, ; McCarthy, Brown, & Bhide, ; Vasconcelos, Stein, & de Almeida, ). Some studies associate genetic changes and the expression of BDNF with the depressive‐like symptoms induced by SD in adult rodents (Berton et al., ; Wook Koo et al., ).…”

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

“…ERK signaling may control transcription by targeting several different regulators of gene expression, such as transcription factors and histone proteins. Activation of the ERK/MAPK pathway could phosphorylate substrates (e.g., CREB) that regulate genes, such as BDNF, which can promote the release of DA, among many other effects (Goggi et al., ; McCarthy et al., ; Vasconcelos et al., ). On the other hand, epigenetic mechanisms induced by social stress could be responsible for the changes observed in DA receptors.…”

Section: Conclusion: Limitations and Future Directionsmentioning

confidence: 99%

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Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Montagud‐Romero

Blanco-Gandía

Reguilón

et al. 2018

Eur J of Neuroscience

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Social interaction is known to be the main source of stress in human beings, which explains the translational importance of this research in animals. Evidence reported over the last decade has revealed that, when exposed to social defeat experiences (brief episodes of social confrontations during adolescence and adulthood), the rodent brain undergoes remodeling and functional modifications, which in turn lead to an increase in the rewarding and reinstating effects of different drugs of abuse. The mechanisms by which social stress cause changes in the brain and behavior are unknown, and so the objective of this review is to contemplate how social defeat stress induces long-lasting consequences that modify the reward system. First of all, we will describe the most characteristic results of the short- and long-term consequences of social defeat stress on the rewarding effects of drugs of abuse such as psychostimulants and alcohol. Secondly, and throughout the review, we will carefully assess the neurobiological mechanisms underlying these effects, including changes in the dopaminergic system, corticotrophin releasing factor signaling, epigenetic modifications and the neuroinflammatory response. To conclude, we will consider the advantages and disadvantages and the translational value of the social defeat stress model, and will discuss challenges and future directions.

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Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

Section: Conclusion: Limitations and Future Directionsmentioning

confidence: 99%

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Montagud‐Romero

Blanco-Gandía

Reguilón

et al. 2018

Eur J of Neuroscience

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“…For instance, California mice show increased anxiety-like behavior immediately prior to a third episode of defeat stress (Greenberg et al , 2015), presumably induced by conditioned stimuli present in the behavior testing room. Sensory contact is an important component of the most widely used protocols for male C57 mice (Golden et al , 2011) and rats (Vasconcelos et al , 2015). This may be because males in these species are more resistant to social defeat.…”

Section: What Is Social Defeat Stress?mentioning

confidence: 99%

Stress, sex, and motivated behaviors

Laman-Maharg

Trainor

2016

J of Neuroscience Research

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Stress is a major risk factor for the development of psychiatric disorders, such as depression, and the development of substance use disorder. Although there are important sex differences in the prevalence of these disorders, the majority of preclinical models used to study stress induced disorders use males only. Social defeat stress is a commonly used method to induce stress in an ethologically relevant way, but has only recently begun to be used in female rodents. Using these new female models, recent studies have examined how social defeat stress affects males and females differently at the behavioral, circuit, and molecular levels. This review discusses sex differences in the effects of social defeat stress on social behavior and drug seeking behavior, as well as its impact on the mesolimbic dopamine system and the highly connected region of the bed nucleus of the stria terminalis.

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“…The influence of chronic stress exposure on affective behaviors has been wellestablished in rats, with a variety of mild, unpredictable, and social stress paradigms able to reduce sucrose preference, as well as increase anxiety-and depression-like behavior (Vasconcelos, Stein, & de Almeida, 2015;Willner, 2017). Alternatively, inherent strain differences in stress susceptibility have presented a challenge towards the use of micean approach that would greatly expand genetic manipulations and cell-specific identification through the use of transgenic animals.…”

Section: Impact Of Stress Intensity and Predictability On Affective Bmentioning

confidence: 99%

Chronic unpredictable stress promotes cell-specific plasticity in prefrontal cortex D1 and D2 pyramidal neurons

Anderson

Gomez

Caccamise

et al. 2019

Preprint

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Exposure to unpredictable environmental stress is widely recognized as a major determinant for risk and severity in neuropsychiatric disorders such as major depressive disorder, anxiety, schizophrenia, and PTSD. The ability of ostensibly unrelated disorders to give rise to seemingly similar psychiatric phenotypes highlights a need to identify circuit-level concepts that could unify diverse factors under a common pathophysiology. Although difficult to disentangle a causative effect of stress from other factors on medial prefrontal cortex (PFC) dysfunction, a wealth of data from humans and rodents demonstrates that the PFC is a key target of stress. The present study sought to identify a model of chronic unpredictable stress (CUS) which induces affective behaviors in C57BL6J mice and once established, measure spike firing and the ability to evoke an action potential in mPFC layer 5/6 pyramidal neurons. Adult male mice received 2 weeks of 'less intense' stress or 2 or 4 weeks of 'more intense' CUS followed by sucrose preference for assessment of anhedonia, elevated plus maze for assessment of anxiety and forced swim test for assessment of depressive-like behaviors. Our findings indicate that more intense CUS exposure results in increased anhedonia, anxiety, and depressive behaviors, while the less intense stress results in no measured behavioral phenotypes. Once a behavioral model was established, mice were euthanized approximately 21 days post-stress for whole-cell patch clamp recordings from layer 5/6 pyramidal neurons in the prelimbic (PrL) and infralimbic (IL) cortices. No significant differences were initially observed in intrinsic cell excitability in either region. However, post-hoc analysis and subsequent confirmation using transgenic mice expressing tdtomato or eGFP under control of dopamine D1-or D2-type receptor showed that D1-expressing pyramidal neurons (D1-PYR) in the PrL exhibit reduced thresholds to fire an action potential (increased excitability) but impaired firing capacity at more depolarized potentials, whereas D2-expressing pyramidal neurons showed an overall reduction in excitability and spike firing frequency. Examination of synaptic transmission showed that D1-and D2-PYR in exhibit differences in basal excitatory and inhibitory signaling under naïve conditions. In CUS mice, D1-PYR showed increased frequency of both miniature excitatory and inhibitory postsynaptic currents, whereas D2-PYR only showed a reduction in excitatory currents. These findings demonstrate that the intrinsic physiology and synaptic regulation of D1-and D2-PYR subpopulations differentially undergo stress-induced plasticity that may have functional implications for stress-related pathology, and that these adaptations may reflect unique differences in basal properties regulating output of these cells.

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Social defeat protocol and relevant biomarkers, implications for stress response physiology, drug abuse, mood disorders and individual stress vulnerability: a systematic review of the last decade

Cited by 51 publications

References 123 publications

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Stress, sex, and motivated behaviors

Chronic unpredictable stress promotes cell-specific plasticity in prefrontal cortex D1 and D2 pyramidal neurons

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