ArticleNeurobiology of stress2020
Blockade of nociceptin/orphanin FQ signaling facilitates an active copying strategy due to acute and repeated stressful stimuli in mice.
Article in Neurobiology of stress, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Genetic Variants Associated With Resilience in Human and Animal Studies.Frontiers in psychiatry · 2022Pooled it
- Integrated Investigation of Sex Differences in the Human Nociceptin/Orphanin FQ Receptor System: Postmortem Analyses and In Vivo [Biological psychiatry. Cognitive neuroscience and neuroimaging · 2026Article
- Duration-Dependent Adverse Events of Systemic Glucocorticosteroids in Atopic Dermatitis: A Nationwide Claims Cohort Study.Dermatology and therapy · 2026Article
- Nociceptin/OrphaninFQ Receptor Modulates the Maturation of Adult-Born Neurons in the Mouse Dentate Gyrus Under Physiological Conditions and in a Chronic Stress Model.Molecular neurobiology · 2025Article
- Adaptation to Preceding Acute Psychological Stress is Associated With Subsequent Stress Coping Levels via Corticoid Receptors.Alpha psychiatry · 2025Article
- Effects of Stress Exposure to Pain Perception in Pre-Clinical Studies: Focus on the Nociceptin/Orphanin FQ-NOP Receptor System.Brain sciences · 2024Review
- Activation of NOP receptor increases vulnerability to stress: role of glucocorticoids and CRF signaling.Psychopharmacology · 2024Article
- BTRX-246040 Acts Through the Ventrolateral Periaqueductal Gray to Exert Antidepressant-Relevant Actions in Mice.The international journal of neuropsychopharmacology · 2023Article
- The role of glucocorticoids in increasing cardiovascular risk.Frontiers in cardiovascular medicine · 2023Article
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of stress in the etiology of depression has been largely reported. In this line, exogenous glucocorticoids are employed to mimic the influence of stress on the development of depression. The N/OFQ-NOP receptor system has been implicated in the modulation of stress and emotional behaviors. In fact, the blockade of NOP receptors induces antidepressant effects and increases resilience to acute stress. This study investigated the effects of the NOP receptor blockade on dexamethasone-treated mice exposed to acute and prolonged swimming stress. Swiss and NOP(+/+) and NOP(-/-) mice were treated with dexamethasone, and the protective effects of the NOP antagonist SB-612111 (10 mg/kg, ip) or imipramine (20 mg/kg, ip) were investigated in three swimming sessions. The re-exposure to swim stress increased immobility time in Swiss and NOP(+/+), but not in NOP(-/-) mice. Acute and repeated dexamethasone administration induced a further increase in the immobility time, and facilitated body weight loss in Swiss mice. Single administration of SB-612111, but not imipramine, prevented swimming stress- and dexamethasone-induced increase in the immobility time. Repeated administrations of SB-612111 prevented the deleterious effects of 5 days of dexamethasone treatment. Imipramine also partially prevented the effects of repeated glucocorticoid administration on the immobility time, but did not affect the body weight loss. NOP(-/-) mice were more resistant than NOP(+/+) mice to inescapable swimming stress, but not dexamethasone-induced increase in the immobility time and body weight loss. In conclusion, the blockade of the NOP receptor facilitates an active stress copying response and attenuates body weight loss due to repeated stress.
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