Social interaction attenuates stress responses following chronic stress in maternally separated rats

Babygirija, Reji; Yoshimoto, Sazu; Gribovskaja‐Rupp, Irena; Bülbül, Mehmet; Ludwig, Kirk; Takahashi, Toshio

doi:10.1016/j.brainres.2012.06.007

Cited by 25 publications

(22 citation statements)

References 57 publications

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“…The trend toward an increase in CORT associated with either OXT treatment or recovery from a stressor in the presence of a partner was not robust. However, the lack of an OXT- or partner-induced reduction in CORT, together with our anatomical data, is not in line with the widely discussed hypothesis, drawn from research in rats (Petersson et al, 1999; Windle et al, 2004, 1997; Babygirija et al, 2012; Blume et al, 2008; Bülbül et al, 2011; Jurek et al, 2015; Zheng et al, 2010), mice made mutant for OXT (Amico et al, 2008), prairie voles (Smith et al, 2015; Smith and Wang, 2014), and humans (Heinrichs et al, 2003; Jong et al, 2015), that OXT and social support exert protective effects primarily by buffering against activation of the HPA axis. Instead, our data suggest that when presented with a stressor that calls for physical and energetic mobilization, administration of exogenous OXT does not prevent what could be an adaptive rise in glucocorticoid levels.…”

Section: Discussioncontrasting

confidence: 93%

Oxytocin promotes functional coupling between paraventricular nucleus and both sympathetic and parasympathetic cardioregulatory nuclei

Yee

Kenkel

Frijling

et al. 2016

Hormones and Behavior

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The neuropeptide oxytocin (OXT) facilitates prosocial behavior and selective sociality. In the context of stress, OXT also can down-regulate hypothalamic–pituitary–adrenal (HPA) axis activity, leading to consideration of OXT as a potential treatment for many socioaffective disorders. However, the mechanisms through which administration of exogenous OXT modulates social behavior in stressful environmental contexts are not fully understood. Here, we investigate the hypothesis that autonomic pathways are components of the mechanisms through which OXT aids the recruitment of social resources in stressful contexts that may elicit mobilized behavioral responses. Female prairie voles (Microtus ochrogaster) underwent a stressor (walking in shallow water) following pretreatment with intraperitoneal OXT (0.25 mg/kg) or OXT antagonist (OXT-A, 20 mg/kg), and were allowed to recover with or without their sibling cagemate. Administration of OXT resulted in elevated OXT concentrations in plasma, but did not dampen the HPA axis response to a stressor. However, OXT, but not OXT-A, pretreatment prevented the functional coupling, usually seen in the absence of OXT, between paraventricular nucleus (PVN) activity as measured by c-Fos immunoreactivity and HPA output (i.e. corticosterone release). Furthermore, OXT pretreatment resulted in functional coupling between PVN activity and brain regions regulating both sympathetic (i.e. rostral ventrolateral medulla) and parasympathetic (i.e. dorsal vagal complex and nucleus ambiguous) branches of the autonomic nervous system. These findings suggest that OXT increases central neural control of autonomic activity, rather than strictly dampening HPA axis activity, and provides a potential mechanism through which OXT may facilitate adaptive and context-dependent behavioral and physiological responses to stressors.

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Section: Discussioncontrasting

confidence: 93%

Oxytocin promotes functional coupling between paraventricular nucleus and both sympathetic and parasympathetic cardioregulatory nuclei

Yee

Kenkel

Frijling

et al. 2016

Hormones and Behavior

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“…Environmental effects during development are well illustrated in animals suffering from trauma in their early development, such as maternal separation [7] or malnutrition [8], thus having a tendency to develop anxiety disorders and presenting physiological changes more easily. A plausible explanation for this is that the hippocampus is more susceptible to adverse influences during the early stages of development.…”

Section: Anxiety Disorders and Bdnfmentioning

confidence: 99%

Translational Findings on Brain-Derived Neurotrophic Factor and Anxiety: Contributions from Basic Research to Clinical Practice

Luz¹,

Dias²,

Bevilaqua³

et al. 2013

Neuropsychobiology

2,969

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Background/Aims: Anxious responses are evolutionarily adaptive, but excessive fear can become disabling and lead to anxiety disorders. Translational models of anxiety might be useful sources for understanding the neurobiology of fear and anxiety and can contribute to future proposals of therapeutic intervention for the disorders studied. Brain-derived neurotrophic factor (BDNF), which is known for its importance on neuroplasticity and contextual memory, has emerged as a relevant element for emotional memory. Recent studies show that the Val⁶⁶Met BDNF polymorphism correlates with various psychiatric disorders, including anxiety, but there are several differences between experimental and clinical studies. Methods: In this work, we review the literature focused on the BDNF Val⁶⁶Met polymorphism and anxiety, and discuss biological findings from animal models to clinical studies. Results: As occurs with other psychiatric disorders, anxiety correlates with anatomical, behavioral and physiological changes related to the BDNF polymorphism. In animal studies, it has been shown that a significant decrease in regulated secretion from both BDNF_Val/Met and BDNF_Met/Met neurons represented a significant decrease in available BDNF. Conclusion: These studies suggest that developing pharmacological strategies facilitating the release of BDNF from synapses or prolongation of the half-life of secreted BDNF may improve the therapeutic responses of humans expressing the BDNF polymorphism.

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“…77 Similar reversal of stress-induced changes in hypothalamic oxytocin mRNA expression was also noted in separated rats housed in mixed conditions. 77 Together these findings suggest that MH may exert its modulatory effect on behaviour by reducing CRH and enhancing oxytocin expression within the hypothalamus, thereby decreasing the magnitude of the HPA response to subsequent stress.…”

Section: Behavioural Interventions Modulate Early Stress-induced Chanmentioning

confidence: 59%

Section: Behavioural Interventions Modulate Early Stress-induced Chanmentioning

confidence: 89%

“…77 Following administration of chronic homotypic stress, MH also reversed the increased CRH mRNA expression and immunoreactivity in the hypothalamus induced by early stress at 8–9 weeks of age. 77 Similar reversal of stress-induced changes in hypothalamic oxytocin mRNA expression was also noted in separated rats housed in mixed conditions. 77 Together these findings suggest that MH may exert its modulatory effect on behaviour by reducing CRH and enhancing oxytocin expression within the hypothalamus, thereby decreasing the magnitude of the HPA response to subsequent stress.…”

Section: Behavioural Interventions Modulate Early Stress-induced Chanmentioning

confidence: 89%

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Modulation of early stress-induced neurobiological changes: a review of behavioural and pharmacological interventions in animal models

Harrison

Baune

2014

Transl Psychiatry

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Childhood adversity alters the predisposition to psychiatric disorders later in life. Those with psychiatric conditions and a history of early adversity exhibit a higher incidence of treatment resistance compared with individuals with no such history. Modulation of the influence early stress exerts over neurobiology may help to prevent the development of psychiatric disorders in some cases, while attenuating the extent of treatment resistance in those with established psychiatric disorders. This review aims to critically evaluate the ability of behavioural, environmental and pharmacologic interventions to modulate neurobiological changes induced by early stress in animal models. Databases were systematically searched to locate literature relevant to this review. Early adversity was defined as stress that resulted from manipulation of the mother–infant relationship. Analysis was restricted to animal models to enable characterisation of how a given intervention altered specific neurobiological changes induced by early stress. A wide variety of changes in neurobiology due to early stress are amenable to intervention. Behavioural interventions in childhood, exercise in adolescence and administration of epigenetic-modifying drugs throughout life appear to best modulate cellar and behavioural alterations induced by childhood adversity. Other pharmacotherapies, such as endocannabinoid system modulators, anti-inflammatories and antidepressants can also influence these neurobiological and behavioural changes that result from early stress, although findings are less consistent at present and require further investigation. Further work is required to examine the influence that behavioural interventions, exercise and epigenetic-modifying drugs exert over alterations that occur following childhood stress in human studies, before possible translational into clinical practice is possible.

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Social interaction attenuates stress responses following chronic stress in maternally separated rats

Cited by 25 publications

References 57 publications

Oxytocin promotes functional coupling between paraventricular nucleus and both sympathetic and parasympathetic cardioregulatory nuclei

Oxytocin promotes functional coupling between paraventricular nucleus and both sympathetic and parasympathetic cardioregulatory nuclei

Translational Findings on Brain-Derived Neurotrophic Factor and Anxiety: Contributions from Basic Research to Clinical Practice

Modulation of early stress-induced neurobiological changes: a review of behavioural and pharmacological interventions in animal models

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