Individual Differences in Reactivity to Social Stress Predict Susceptibility and Resilience to a Depressive Phenotype: Role of Corticotropin-Releasing Factor

Wood, Susan K.; Walker, Hayley; Valentino, Rita J.; Bhatnagar, Seema

doi:10.1210/en.2009-1026

Cited by 210 publications

(318 citation statements)

References 52 publications

Supporting

Mentioning

283

Contrasting

Unclassified

Order By: Relevance

“…As previously reported (Wood et al, 2010), rats exposed to repeated social stress clustered into two populations based on their latency to assume the defeat posture, with a mean latency of 305 s ± 24 s for SL rats (n = 13) and a mean latency of 560 ± 20 s for LL rats (n = 14) (po0.001). Analyzing CRF effects with respect to coping style revealed that social stress shifted the CRF response from improvement of strategy shifting to improvement of reversal learning selectively in LL rats (Figure 5b).…”

Section: Impact Of Prior Social Stress Experience On the Cognitive Efsupporting

confidence: 61%

“…CRF-related plasticity in the DRN may be one mechanism for this shift. The finding that this adaptation is most apparent in the LL subpopulation, the population that is relatively resistant to developing depression-related endocrine, behavioral and cardiovascular endpoints suggests links between coping style and the cognitive consequences of stress (Wood et al, 2010(Wood et al, , 2012.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Corticotropin-releasing Factor in the Rat Dorsal Raphe Nucleus Promotes Different Forms of Behavioral Flexibility Depending on Social Stress History

Snyder

Hill-Smith

Lucki

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

The stress-related neuropeptide, corticotropin-releasing factor (CRF) regulates the dorsal raphe nucleus-serotonin (DRN-5-HT) system during stress and this may underlie affective and cognitive dysfunctions that characterize stress-related psychiatric disorders. CRF acts on both CRF 1 and CRF 2 receptor subtypes in the DRN that exert opposing inhibitory and excitatory effects on DRN-5-HT neuronal activity and 5-HT forebrain release, respectively. The current study first assessed the cognitive effects of intra-DRN microinfusion of CRF or the selective CRF 2 agonist, urocortin II in stress-naive rats on performance of an operant strategy set-shifting task that is mediated by the medial prefrontal cortex (mPFC). CRF (30 ng) facilitated strategy set-shifting performance, whereas higher doses of CRF and urocortin II that would interact with CRF 2 were without effect, consistent with a CRF 1 -mediated action. This dose decreased 5-HT extracellular levels in the mPFC, further supporting a role for CRF 1 . The effects of CRF were then assessed in rats exposed to repeated social stress using the resident-intruder model. Repeated social stress shifted the CRF effect from facilitation of strategy set shifting to facilitation of reversal learning and this was most prominent in a subpopulation of rats that resist defeat. Notably, in this subpopulation of rats 5-HT neuronal responses to CRF have been demonstrated to shift from CRF 1 -mediated inhibition to CRF 2 -mediated excitation. Because 5-HT facilitates reversal learning, the present results suggest that stress-induced changes in the cellular effects of CRF in the DRN translate to changes in cognitive effects of CRF. Together, the results underscore the potential for stress history to shift cognitive processing through changes in CRF neurotransmission in the DRN and the association of this effect with coping strategy.

show abstract

Section: Impact Of Prior Social Stress Experience On the Cognitive Efsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing Factor in the Rat Dorsal Raphe Nucleus Promotes Different Forms of Behavioral Flexibility Depending on Social Stress History

Snyder

Hill-Smith

Lucki

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Following post-surgical recovery, rats were exposed to either resident-intruder stress (Miczek, 1979) or control manipulation, as described previously (Wood et al, 2010). Intruders were placed into the resident's cage.…”

Section: Repeated Social Stressmentioning

confidence: 99%

“…Human social stress is modeled in rodents using the resident-intruder model (Miczek, 1979). Adult male rats repeatedly exposed to resident-intruder stress display endocrine, autonomic and behavioral features that characterize mood disorders in humans, underscoring the potential of this model to produce correlates of stress-related psychiatric diseases Rygula et al, 2005;Wood et al, 2010Wood et al, , 2012Wood et al, , 2013. Although less well studied, adolescent male rats exposed to repeated resident-intruder stress have been reported to have cognitive impairments and escalated cocaine self-administration when tested in adulthood (Burke and Miczek, 2015;Novick et al, 2013;Snyder et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Adolescent Social Stress Produces an Enduring Activation of the Rat Locus Coeruleus and Alters its Coherence with the Prefrontal Cortex

Zitnik

Curtis

Wood

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

Early life stress is associated with the development of psychiatric disorders. Because the locus coeruleus-norepinephrine (LC-NE) system is a major stress-response system that is implicated in psychopathology, developmental differences in the response of this system to stress may contribute to increased vulnerability. Here LC single unit and network activity were compared between adult and adolescent rats during resident-intruder stress. In some rats, LC and medial prefrontal cortex (mPFC) coherence was quantified. The initial stress tonically activated LC neurons and induced theta oscillations, while simultaneously decreasing LC auditory-evoked responses in both age groups. Stress increased LC-mPFC coherence within the theta range. With repeated exposures, adolescent LC neuronal and network activity remained elevated even in the absence of the stressor and were unresponsive to stressor presentation. In contrast, LC neurons of adult rats exposed to repeated social stress were relatively inhibited in the absence of the stressor and mounted robust responses upon stressor presentation. LC sensory-evoked responses were selectively blunted in adolescent rats exposed to repeated social stress. Finally, repeated stress decreased LC-mPFC coherence in the high frequency range (beta and gamma) while maintaining strong coherence in the theta range, selectively in adolescents. Together, these results suggest that adaptive mechanisms that promote stress recovery and maintain basal activity of the brain norepinephrine system in the absence of stress are not fully developed or are vulnerable stress-induced impairments in adolescence. The resulting sustained activation of the LC-NE system after repeated social stress may adversely impact cognition and future social behavior of adolescents.

show abstract

“…These differential responses, including determining susceptibility versus resilience to stress, contribute to the pathophysiology of debilitating stress-related disorders (2)(3)(4)(5). The hippocampus is a brain region noted for its plasticity in response to stress and sensitivity to adrenal steroid hormones (6).…”

mentioning

confidence: 99%

Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity

Nasca

Zelli

Bigio

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

121

View full text Add to dashboard Cite

Excitatory amino acids play a key role in both adaptive and deleterious effects of stressors on the brain, and dysregulated glutamate homeostasis has been associated with psychiatric and neurological disorders. Here, we elucidate mechanisms of epigenetic plasticity in the hippocampus in the interactions between a history of chronic stress and familiar and novel acute stressors that alter expression of anxiety-and depressive-like behaviors. We demonstrate that acute restraint and acute forced swim stressors induce differential effects on these behaviors in naive mice and in mice with a history of chronic-restraint stress (CRS). They reveal a key role for epigenetic up-and down-regulation of the putative presynaptic type 2 metabotropic glutamate (mGlu2) receptors and the postsynaptic NR1/NMDA receptors in the hippocampus and particularly in the dentate gyrus (DG), a region of active neurogenesis and a target of antidepressant treatment. We show changes in DG long-term potentiation (LTP) that parallel behavioral responses, with habituation to the same acute restraint stressor and sensitization to a novel forced-swim stressor. In WT mice after CRS and in unstressed mice with a BDNF loss-of-function allele (BDNF Val66Met), we show that the epigenetic activator of histone acetylation, P300, plays a pivotal role in the dynamic up-and down-regulation of mGlu2 in hippocampus via histone-3-lysine-27-acetylation (H3K27Ac) when acute stressors are applied. These hippocampal responses reveal a window of epigenetic plasticity that may be useful for treatment of disorders in which glutamatergic transmission is dysregulated.S tress effects on higher brain regions, such as hippocampus, are known to involve actions of excitatory amino acids to induce structural and functional changes depending upon the type, intensity, and duration of the stressor (1). These differential responses, including determining susceptibility versus resilience to stress, contribute to the pathophysiology of debilitating stress-related disorders (2-5). The hippocampus is a brain region noted for its plasticity in response to stress and sensitivity to adrenal steroid hormones (6). Acute stress enhances synaptic plasticity that is associated with improved cognition and other adaptive functions whereas chronic stress produces opposite effects mediating, in the hippocampus, spine synapse turnover, dendritic shrinkage, impaired long-term potentiation (LTP), and suppression of adult neurogenesis in the dentate gyrus (DG) (1, 7). Importantly, neuroanatomical changes in response to repeated stress recover in young adult animals, based upon the restoration of dendritic length and branching and spine density (8). However, there are underlying changes that can be seen at the level of gene expression and epigenetic regulation that indicate that the brain is continually changing (9, 10). Epigenetic modifications, such as acetylation of histones, have also been involved in the consolidation of contextual memories that allow the brain to respond and adapt to changes in ...

show abstract

Individual Differences in Reactivity to Social Stress Predict Susceptibility and Resilience to a Depressive Phenotype: Role of Corticotropin-Releasing Factor

Cited by 210 publications

References 52 publications

Corticotropin-releasing Factor in the Rat Dorsal Raphe Nucleus Promotes Different Forms of Behavioral Flexibility Depending on Social Stress History

Corticotropin-releasing Factor in the Rat Dorsal Raphe Nucleus Promotes Different Forms of Behavioral Flexibility Depending on Social Stress History

Adolescent Social Stress Produces an Enduring Activation of the Rat Locus Coeruleus and Alters its Coherence with the Prefrontal Cortex

Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity

Contact Info

Product

Resources

About