Corticotropin‐releasing factor receptor type 2‐deficient mice display impaired coping behaviors during stress

Coste, Sarah C.; Heard, Amanda; Phillips, Tamara J.; Stenzel-Poore, Mary P.

doi:10.1111/j.1601-183x.2005.00142.x

Cited by 29 publications

(20 citation statements)

References 54 publications

(110 reference statements)

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“…The present findings of decreased somatic opiate withdrawal signs in CRF 2 À/À mice are in apparent contrast with studies showing that CRF 2 À/À mice displayed increased behavioral responses to stressful events (Bale et al, 2000;Bale and Vale, 2003;Coste et al, 2006;Kishimoto et al, 2000). However, in contrast to CRF 1 receptors, the role for the CRF 2 receptor pathway in stress-responsive circuitry is somewhat less clear.…”

Section: Discussioncontrasting

confidence: 99%

“…In particular, CRF 1 receptordeficient mice display decreased hypothalamus-pituitaryadrenal (HPA) axis as well as behavioral reactions to stressors (Contarino et al, 1999;Muller et al, 2003;Smith et al, 1998;Timpl et al, 1998). In net contrast, CRF 2 receptor-deficient mice show increased HPA axis and affective-like responses to stressors (Bale et al, 2000;Bale and Vale, 2003;Coste et al, 2000Coste et al, , 2006Kishimoto et al, 2000). In line with a major role for the CRF 1 receptor pathway in stress-responsive circuitry, we found that genetic disruption of the CRF 1 receptor pathway eliminated the negative affective-like states of opiate withdrawal (Contarino and Papaleo, 2005).…”

Section: Introductionmentioning

confidence: 54%

“…Also, CRF 1 À/À mice displayed deficient HPA axis responses to stressful events (Contarino and Papaleo, 2005;Papaleo et al, 2007;Smith et al, 1998;Timpl et al, 1998). In net contrast, genetic disruption of the CRF 2 receptor pathway increased the expression of anxiety-like and depression-like behavior, and exacerbated HPA axis responses to an immobilization stress (Bale et al, 2000;Bale and Vale, 2003;Coste et al, 2000Coste et al, , 2006Kishimoto et al, 2000). Finally, CRF 1 and CRF 2 receptor pathways were shown to have opposite roles on information processing mechanisms that regulate responses to stressors.…”

Section: Discussionmentioning

confidence: 98%

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Disruption of the CRF2 Receptor Pathway Decreases the Somatic Expression of Opiate Withdrawal

Papaleo

Ghozland

Ingallinesi

et al. 2008

Neuropsychopharmacol

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Escape from the extremely aversive opiate withdrawal symptoms powerfully motivates compulsive drug-seeking and drug-taking behaviors. The corticotropin-releasing factor (CRF) system is hypothesized to mediate the motivational properties of drug dependence. CRF signaling is transmitted by two receptor pathways, termed CRF 1 and CRF 2 . To investigate the role for the CRF 2 receptor pathway in somatic opiate withdrawal, in the present study we used genetically engineered mice deficient in the CRF 2 receptor (CRF 2 À/À). We employed a novel, clinically relevant mouse model of 'spontaneous' opiate withdrawal as well as a classical opioid receptor antagonist (naloxone)-precipitated opiate withdrawal paradigm. To induce opiate dependence, mice were treated with intermittent escalating morphine doses (20-100 mg/kg, i.p.). We found that 8-128 h after the last opiate injection, CRF 2 À/À mice showed decreased levels of major somatic signs of spontaneous opiate withdrawal, such as paw tremor and wet dog shake, as compared to wild-type mice. Similarly, challenge with naloxone 2 h after the last morphine injection induced lower levels of paw tremor and wet dog shake in CRF 2 À/À mice as compared to wild-type mice. Despite the differences in somatic signs, wild-type and CRF 2 À/À mice displayed similar plasma corticosterone responses to opiate dosing and withdrawal, indicating a marginal role for the hypothalamus-pituitary-adrenal axis in the CRF 2 receptor mediation of opiate withdrawal. Our results unravel a novel role for the CRF 2 receptor pathway in opiate withdrawal. The CRF 2 receptor pathway might be a critical target of therapies aimed at alleviating opiate withdrawal symptoms and reducing relapse to drug intake.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 98%

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Disruption of the CRF2 Receptor Pathway Decreases the Somatic Expression of Opiate Withdrawal

Papaleo

Ghozland

Ingallinesi

et al. 2008

Neuropsychopharmacol

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“…29 Extrahypothalamic distribution of CRF includes neuronal populations in the amygdala, 30,31 hippocampus, 32 and locus coeruleus. 33 CRF and its related peptides exert central function and mediate several behavioral and physiological responses to stress, [34][35][36][37][38] including anxiety-like behavior and some aspects of aggressiveness. 35,[39][40][41][42][43] The present study tested the hypothesis that BDNF may underlie, at least in part, experience-induced neuroplasticity in resident mice exposed to repeated sessions of agonistic interactions.…”

Section: Introductionmentioning

confidence: 99%

“…33 CRF and its related peptides exert central function and mediate several behavioral and physiological responses to stress, [34][35][36][37][38] including anxiety-like behavior and some aspects of aggressiveness. 35,[39][40][41][42][43] The present study tested the hypothesis that BDNF may underlie, at least in part, experience-induced neuroplasticity in resident mice exposed to repeated sessions of agonistic interactions. BDNF is a molecule involved in the regulation of diverse biological functions, ranging from neuronal survival and differentiation during development to synaptic plasticity and cognitive behavior in the adult 44 ; it has also been demonstrated to be a critical mediator of changes in social motivation.…”

Section: Introductionmentioning

confidence: 99%

Social instigation and repeated aggressive confrontations in male Swiss mice: analysis of plasma corticosterone, CRF and BDNF levels in limbic brain areas

Fortes

Albrechet‐Souza

Vasconcelos

et al. 2017

Trends Psychiatry Psychother.

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Introduction: Agonistic behaviors help to ensure survival, provide advantage in competition, and communicate social status. The resident-intruder paradigm, an animal model based on male intraspecific confrontations, can be an ethologically relevant tool to investigate the neurobiology of aggressive behavior. Objectives: To examine behavioral and neurobiological mechanisms of aggressive behavior in male Swiss mice exposed to repeated confrontations in the resident intruder paradigm. Methods: Behavioral analysis was performed in association with measurements of plasma corticosterone of mice repeatedly exposed to a potential rival nearby, but inaccessible (social instigation), or to 10 sessions of social instigation followed by direct aggressive encounters. Moreover, corticotropin-releasing factor (CRF) and brain-derived neurotrophic factor (BNDF) were measured in the brain of these animals. Control mice were exposed to neither social instigation nor aggressive confrontations. Results: Mice exposed to aggressive confrontations exhibited a similar pattern of species-typical aggressive and non-aggressive behaviors on the first and the last session. Moreover, in contrast to social instigation only, repeated aggressive confrontations promoted an increase in plasma corticosterone. After 10 aggressive confrontation sessions, mice presented a non-significant trend toward reducing hippocampal levels of CRF, which inversely correlated with plasma corticosterone levels. Conversely, repeated sessions of social instigation or aggressive confrontation did not alter BDNF concentrations at the prefrontal cortex and hippocampus. Conclusion: Exposure to repeated episodes of aggressive encounters did not promote habituation over time. Additionally, CRF seems to be involved in physiological responses to social stressors.

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Aggression in non‐human vertebrates: Genetic mechanisms and molecular pathways

Freudenberg

Gutiérrez

Post

et al. 2015

American J of Med Genetics Pt B

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Aggression is an adaptive behavioral trait that is important for the establishment of social hierarchies and competition for mating partners, food, and territories. While a certain level of aggression can be beneficial for the survival of an individual or species, abnormal aggression levels can be detrimental. Abnormal aggression is commonly found in human patients with psychiatric disorders. The predisposition to aggression is influenced by a combination of environmental and genetic factors and a large number of genes have been associated with aggression in both human and animal studies. In this review, we compare and contrast aggression studies in zebrafish and mouse. We present gene ontology and pathway analyses of genes linked to aggression and discuss the molecular pathways that underpin agonistic behavior in these species.

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Corticotropin‐releasing factor receptor type 2‐deficient mice display impaired coping behaviors during stress

Cited by 29 publications

References 54 publications

Disruption of the CRF2 Receptor Pathway Decreases the Somatic Expression of Opiate Withdrawal

Disruption of the CRF2 Receptor Pathway Decreases the Somatic Expression of Opiate Withdrawal

Social instigation and repeated aggressive confrontations in male Swiss mice: analysis of plasma corticosterone, CRF and BDNF levels in limbic brain areas

Aggression in non‐human vertebrates: Genetic mechanisms and molecular pathways

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