Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress

Lowrance, Steven Allen; Ionadi, Amy; McKay, Erin; Douglas, Xavier; Johnson, John D.

doi:10.1016/j.psyneuen.2016.02.027

Cited by 67 publications

(46 citation statements)

References 66 publications

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“…It is currently unknown whether chronic stress directly affects GR levels in aged mice ( Gjerstad et al, 2018 ; Mifsud and Reul, 2018 ). In the present study, stress elevated the corticosterone level in the blood, which is consistent with the results of a previously described study ( Lowrance et al, 2016 ). Necrostatin-1 had no effect on the corticosterone level in stressed mice.…”

Section: Discussionsupporting

confidence: 94%

Inhibiting RIP1 Improves Chronic Stress-Induced Cognitive Impairments in D-Galactose-Induced Aging Mice

Wang

et al. 2018

Front. Behav. Neurosci.

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Mounting evidence shows that chronic stress can affect both the structure and function of the brain resulting in decreased synaptic plasticity and cognitive dysfunction. Although several studies have indicated that aged brains are more vulnerable to chronic stress, it remains unknown how to prevent stress-induced memory deficits in aged animals. Neuroinflammation plays an important role in the pathogenesis of chronic stress-related brain dysfunction. Receptor-interacting protein 1 (RIP1) is a key molecule that can modulate inflammation, apoptosis, and necroptosis. Here, we investigated whether inhibiting RIP1 using necrostatin-1 during chronic stress could improve chronic stress-related brain dysfunction in D-galactose-induced aging mice. The stressed mice underwent restraint stress for 14 days. Necrostatin-1 (6.25 mg/kg) or vehicle was administered intraperitoneally once every 3 days during the stress period. Locomotor activity was tested using the open field test and cognitive function was assessed using the novel object recognition and Barnes maze tests. The hippocampus was collected to assess neuroinflammation (Iba1, IL-1α, IL-1β, TNF-α, and C1q), necroptosis [RIP1, RIP3, mixed lineage kinase domain-like (MLKL), and NF-κB], neuroplasticity (doublecortin, NR1, NR2A, NR2B, GluA1, and GluA2), and the expression of glucocorticoid and mineralocorticoid receptors. Blood samples were collected to quantify the levels of corticosterone. We found that chronic stress induced obvious memory impairment and neuroinflammation, decreased neurogenesis and GluA2 expression, and increased the expression of RIP1 and NF-κB. Inhibiting RIP1 by necrostatin-1 during chronic stress rescued the memory impairment and alleviated the pathological changes induced by stress. These suggest that inhibiting RIP1 using necrostatin-1 improves chronic stress-related brain dysfunction in D-galactose-induced aging mice. The potential mechanisms include limitation of neuroinflammation and the rescue of neurogenesis and GluA2 expression.

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Section: Discussionsupporting

confidence: 94%

Inhibiting RIP1 Improves Chronic Stress-Induced Cognitive Impairments in D-Galactose-Induced Aging Mice

Wang

et al. 2018

Front. Behav. Neurosci.

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“…7C, IPETT), indicating that physical exercise and stress training had differences in regulating EPI sensitivity of blood glucose. Studies have shown that chronic stress increased sympathetic nervous activity and elevated basal corticosterone levels and rapid glucocorticoid production (Lowrance et al, 2016). However, chronic exercise enhanced HPA-axis negative feedback and thus reduced HPA responses to stress or next bout of exercise (Hare et al, 2014).…”

Section: Myonectin Kncokdown Reverses the Beneficial Effects Of Stresmentioning

confidence: 99%

“…Chronic stress and exercise are both important exogenous factors to induce the activation of HPA axis. Chronic stress increased sympathetic nervous activity and elevated basal corticosterone levels and rapid glucocorticoid production, so stress exposure increases blood glucose via the activation of HPA axis (Lowrance et al, 2016). However, chronic exercise enhanced HPA-axis negative feedback and thus reduced HPA responses to stress or next bout of exercise (Hare et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Stress-induced myonectin improves glucose homeostasis by inhibiting glycemic response to HPA axis

Zhang

Xia

Xue

et al. 2019

Preprint

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One Sentence Summary: Chronic stress breaks glucose intolerance cycle to resist diet-induced obesity, through myonectin-mediated inhibition of glycemic response to epinephrine (EPI) and activation of insulin signaling in adipose tissues. GraphicalAbstract Stress AAV+ Sympathetic output HFD 2wk Glucose intolerance 4wk Insulin sensitivity ↓ EPI sensitivity ↑ 3wk Glucose intolerance↑ Insulin sensitivity↑ Insulin sensitivity↑↑ P-Akt Ser473↑ EPI sensitivity↑ Thermogenesis↑ Insulin sensitivity↑ P-Akt Ser473↑ EPI sensitivity↑ Lipolysis↑ Myonectin↑ BAT WAT Improved Glycemic Control Stress diet Improved Metabolic Profile Glucose Intolerance Cycle ? ? Obesity Highlights  EPI sensitivity increases after glucose intolerance and with reduced insulin sensitivity in diet-induced obesity  Chronic stress blunts glycemic responses to EPI and increases myonectin levels in serum and skeletal muscle  Myonectin attenuates glycemic response to EPI and improves metabolic profile in HFD-fed mice  Reducing myonectin reverses beneficial effects of stress on glucose homeostasis AbstractInhibiting glycemic response to HPA axis contributes to glycemic control for diabetic patients.Here, mice were subjected to high-fat diet and intermittent chronic stress, and glucose homeostasis and lipolysis were determined during the intervention. Firstly, we found that glucose intolerance appears at the earliest, followed by reduced insulin sensitivity and increased epinephrine (EPI) sensitivity in the early stage of diet-induced obesity. Next we investigated whether chronic stress impairs glycemic control and which mediates its effects. Short-term stress training raises serum and skeletal muscle myonectin (Myn) levels and improves glucose intolerance. Stress attenuates blood glucose and glycerol responses to EPI, but enhances lipolytic response to EPI in adipose tissues. Myn overexpression in vivo improves glucose tolerance and enhances insulin sensitivity at the cost of blunting glycemic responses to EPI. Myn knockdown reduces beneficial effects of stress or exercise on glucose homeostasis. Together, myonectin is a stress-induced myokine that readjusts glycemic and metabolic responses to HPA axis, and thus prevent the progression of glucose intolerance and obesity. Clin Endocrinol Metab 92(7): JS, Samuel VT (2014) Targeting steroid receptor coactivator 1 with antisense oligonucleotides increases insulin-stimulated skeletal muscle glucose uptake in chow-fed and high-fat-fed male rats. Am J Physiol Endocrinol Metab 307(9): E773-E783 Chuang JC, Krishnan V, Yu HG, Mason B, Cui H, Wilkinson MB, Zigman JM, Elmquist JK, Nestler EJ, Lutter M (2010) A beta3-adrenergic-leptin-melanocortin circuit regulates behavioral and metabolic changes induced by chronic stress. Biol Psychiatry 67(11): 1075-1082 Covington JD, Tam CS, Bajpeyi S, Galgani JE, Noland RC, Smith SR, Redman LM, Ravussin E (2016) Myokine Expression in Muscle and Myotubes in Response to Exercise Stimulation. Med Sci Sports Exerc 48(3): 384-390 Crunkhorn S (2018) Metabolic disease: Safely mimicking c...

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“…Activation of these systems may be associated with altered behavior [4], hormonal signaling [5] as well as changes in the immune system, for review see [6]. Environmental stressors may promote myelopoiesis in the bone marrow [7], glucocorticoid (GC) resistance in the brain and the spleen [8], increased circulatory levels of cytokines [9] and altered inflammatory profile in the brain [10].…”

Section: Introductionmentioning

confidence: 99%

Repeated social defeat promotes persistent inflammatory changes in splenic myeloid cells; decreased expression of β-arrestin-2 (ARRB2) and increased expression of interleukin-6 (IL-6)

Rajalingam

Nymoen²,

Jacobsen³

et al. 2020

Preprint

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Background Previous studies suggest that persistent exposure to social stress in mammals may be associated with multiple physiological effects. Here, we examine the effects of social stress in rats, i.e. repeated social defeat, on behavior, hypothalamic-pituitary-adrenal (HPA)-axis and immune system. Methods A resident-intruder paradigm, where an intruder rat was exposed to social stress by a dominant resident rat for one hour each day for seven consecutive days was used. The day after the last stress exposure in the paradigm the data were analyzed. Variation in social interaction was observed manually, whereas locomotion was analyzed off-line by a purpose-made software. Gene expression in the pituitary gland, adrenal gland and myeloid cells isolated from the spleen was measured by qPCR. Results The exposure to social stress induced decreased weight gain and increased locomotion. An increased nuclear receptor subfamily group C number 1 (NR3C1) expression in the pituitary gland was also shown. In myeloid cells harvested from the spleen, we observed decreased expression of the β 2 -adrenergic receptor (ADRB2) and β-arrestin-2 (ARRB2), but increased expression of interleukin-6 (IL-6). Subsequent analyses in the same cells showed that ARRB2 was negatively correlated with IL-6 following the stress exposure. Conclusion Our results show that that the experience of social stress in the form of repeated social defeat in rats is a potent stressor that in myeloid cells in the spleen promotes persistent inflammatory changes. Future research is needed to examine whether similar inflammatory changes also can explain the impact of social stress, such as bullying and harassment, among humans.

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Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress

Cited by 67 publications

References 66 publications

Inhibiting RIP1 Improves Chronic Stress-Induced Cognitive Impairments in D-Galactose-Induced Aging Mice

Inhibiting RIP1 Improves Chronic Stress-Induced Cognitive Impairments in D-Galactose-Induced Aging Mice

Stress-induced myonectin improves glucose homeostasis by inhibiting glycemic response to HPA axis

Repeated social defeat promotes persistent inflammatory changes in splenic myeloid cells; decreased expression of β-arrestin-2 (ARRB2) and increased expression of interleukin-6 (IL-6)

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