Effects of Animal Care Procedures on Plasma Corticosterone Levels in Group-Housed Mice during the Nocturnal Active Phase

Sakakibara, Hiroyuki; Koyanagi, Akiharu; Suzuki, Tatsuo; Suzuki, Atsumi; Lin, Ling; Shimoi, Kayoko

doi:10.1538/expanim.59.637

Cited by 11 publications

(10 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We therefore measured plasma corticosterone levels in animals that had breathed air or 5% CO 2 in air for 30 min. Plasma corticosterone levels have been shown to rise when animals are stressed ( Aliczki et al , 2013 ; Sakakibara et al , 2010 ). There was no difference in the plasma corticosterone levels in animals breathing air or 5% CO 2 in air (233.7±23.1 and 229.2±34.6 ng/ml, respectively, N =10).…”

Section: Resultsmentioning

confidence: 99%

Ethanol Reversal of Tolerance to the Respiratory Depressant Effects of Morphine

Hill

Lyndon

Withey

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

Opioids are the most common drugs associated with unintentional drug overdose. Death results from respiratory depression. Prolonged use of opioids results in the development of tolerance but the degree of tolerance is thought to vary between different effects of the drugs. Many opioid addicts regularly consume alcohol (ethanol), and post-mortem analyses of opioid overdose deaths have revealed an inverse correlation between blood morphine and ethanol levels. In the present study, we determined whether ethanol reduced tolerance to the respiratory depressant effects of opioids. Mice were treated with opioids (morphine, methadone, or buprenorphine) for up to 6 days. Respiration was measured in freely moving animals breathing 5% CO2 in air in plethysmograph chambers. Antinociception (analgesia) was measured as the latency to remove the tail from a thermal stimulus. Opioid tolerance was assessed by measuring the response to a challenge dose of morphine (10 mg/kg i.p.). Tolerance developed to the respiratory depressant effect of morphine but at a slower rate than tolerance to its antinociceptive effect. A low dose of ethanol (0.3 mg/kg) alone did not depress respiration but in prolonged morphine-treated animals respiratory depression was observed when ethanol was co-administered with the morphine challenge. Ethanol did not alter the brain levels of morphine. In contrast, in methadone- or buprenorphine-treated animals no respiratory depression was observed when ethanol was co-administered along with the morphine challenge. As heroin is converted to morphine in man, selective reversal of morphine tolerance by ethanol may be a contributory factor in heroin overdose deaths.

show abstract

Section: Resultsmentioning

confidence: 99%

Ethanol Reversal of Tolerance to the Respiratory Depressant Effects of Morphine

Hill

Lyndon

Withey

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Stress-relative responses in rodents under stressful conditions can be evaluated by measuring plasma levels of corticosterone and NORA (main circulating glucocorticoid and catecholamine, respectively) [32,33]. As shown in Figure 1.…”

Section: Resultsmentioning

confidence: 99%

Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6- and glutathione-dependent mechanism

et al. 2013

View full text Add to dashboard Cite

BackgroundInterleukin (IL)-6 (mainly of tumor origin) activates glutathione (GSH) release from hepatocytes and its interorgan transport to B16-F10 melanoma metastatic foci. We studied if this capacity to overproduce IL-6 is regulated by cancer cell-independent mechanisms.MethodsMurine B16-F10 melanoma cells were cultured, transfected with red fluorescent protein, injected i.v. into syngenic C57BL/6J mice to generate lung and liver metastases, and isolated from metastatic foci using high-performance cell sorting. Stress hormones and IL-6 levels were measured by ELISA, and CRH expression in the brain by in situ hybridization. DNA binding activity of NF-κB, CREB, AP-1, and NF-IL-6 was measured using specific transcription factor assay kits. IL-6 expression was measured by RT-PCR, and silencing was achieved by transfection of anti-IL-6 small interfering RNA. GSH was determined by HPLC. Cell death analysis was distinguished using fluorescence microscopy, TUNEL labeling, and flow cytometry techniques. Statistical analyses were performed using Student’s t test.ResultsPlasma levels of stress-related hormones (adrenocorticotropin hormone, corticosterone, and noradrenaline) increased, following a circadian pattern and as compared to non-tumor controls, in mice bearing B16-F10 lung or liver metastases. Corticosterone and noradrenaline, at pathophysiological levels, increased expression and secretion of IL-6 in B16-F10 cells in vitro. Corticosterone- and noradrenaline-induced transcriptional up-regulation of IL-6 gene involves changes in the DNA binding activity of nuclear factor-κB, cAMP response element-binding protein, activator protein-1, and nuclear factor for IL-6. In vivo inoculation of B16-F10 cells transfected with anti-IL-6-siRNA, treatment with a glucocorticoid receptor blocker (RU-486) or with a β-adrenoceptor blocker (propranolol), increased hepatic GSH whereas decreased plasma IL-6 levels and metastatic growth. Corticosterone, but not NORA, also induced apoptotic cell death in metastatic cells with low GSH content.ConclusionsOur results describe an interorgan system where stress-related hormones, IL-6, and GSH coordinately regulate metastases growth.

show abstract

“…As such, rhythms in arousal will influence where an individual sits on the arousal-performance curve, and are likely to contribute to the rhythms seen in behavioral performance in animal studies. As a result of the differences in baseline arousal, the response to stressors such as handling, restraint, and environmental noise will differ ( 162 , 163 ). When baseline arousal is low, increased arousal may be expected to result in improved performance, but when baseline arousal is high, increasing arousal further may impair performance (Figure 3 ).…”

Section: Cognitionmentioning

confidence: 99%

Light and Cognition: Roles for Circadian Rhythms, Sleep, and Arousal

et al. 2018

View full text Add to dashboard Cite

Light exerts a wide range of effects on mammalian physiology and behavior. As well as synchronizing circadian rhythms to the external environment, light has been shown to modulate autonomic and neuroendocrine responses as well as regulating sleep and influencing cognitive processes such as attention, arousal, and performance. The last two decades have seen major advances in our understanding of the retinal photoreceptors that mediate these non-image forming responses to light, as well as the neural pathways and molecular mechanisms by which circadian rhythms are generated and entrained to the external light/dark (LD) cycle. By contrast, our understanding of the mechanisms by which lighting influences cognitive processes is more equivocal. The effects of light on different cognitive processes are complex. As well as the direct effects of light on alertness, indirect effects may also occur due to disrupted circadian entrainment. Despite the widespread use of disrupted LD cycles to study the role circadian rhythms on cognition, the different experimental protocols used have subtly different effects on circadian function which are not always comparable. Moreover, these protocols will also disrupt sleep and alter physiological arousal, both of which are known to modulate cognition. Studies have used different assays that are dependent on different cognitive and sensory processes, which may also contribute to their variable findings. Here, we propose that studies addressing the effects of different lighting conditions on cognitive processes must also account for their effects on circadian rhythms, sleep, and arousal if we are to fully understand the physiological basis of these responses.

show abstract

Effects of Animal Care Procedures on Plasma Corticosterone Levels in Group-Housed Mice during the Nocturnal Active Phase

Cited by 11 publications

References 22 publications

Ethanol Reversal of Tolerance to the Respiratory Depressant Effects of Morphine

Ethanol Reversal of Tolerance to the Respiratory Depressant Effects of Morphine

Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6- and glutathione-dependent mechanism

Light and Cognition: Roles for Circadian Rhythms, Sleep, and Arousal

Contact Info

Product

Resources

About