ArticleCellular and molecular neurobiology2012
Assessing behavioural effects of chronic HPA axis activation using conditional CRH-overexpressing mice.
Article in Cellular and molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed.
- Paternal Caffeine Exposure Programs Offspring Stress Vulnerability via Sperm Dlk1-Dio3 Imprinting-Directed Remodeling of a Novel Neural Circuit.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Systemic and cardiac pathology induced by a clinically relevant USP8 activating mutation.Disease models & mechanisms · 2026Article
- Selective and differential roles of PVHNature communications · 2026Article
- Cushing's Disease in the Animal Kingdom: Translational Insights for Human Medicine.International journal of molecular sciences · 2025Review
- Deletion of CRH From GABAergic Forebrain Neurons Promotes Stress Resilience and Dampens Stress-Induced Changes in Neuronal Activity.Frontiers in neuroscience · 2019Article
- MARCKSL1 Regulates Spine Formation in the Amygdala and Controls the Hypothalamic-Pituitary-Adrenal Axis and Anxiety-Like Behaviors.EBioMedicine · 2018Article
- Cross-disorder risk gene CACNA1C differentially modulates susceptibility to psychiatric disorders during development and adulthood.Molecular psychiatry · 2018Article
- NRSF-dependent epigenetic mechanisms contribute to programming of stress-sensitive neurons by neonatal experience, promoting resilience.Molecular psychiatry · 2018Article
- The CRF Family of Neuropeptides and their Receptors - Mediators of the Central Stress Response.Current molecular pharmacology · 2018Review
- Energetic stress: The reciprocal relationship between energy availability and the stress response.Physiology & behavior · 2016Review
- Sustained glucocorticoid exposure recruits cortico-limbic CRH signaling to modulate endocannabinoid function.Psychoneuroendocrinology · 2016Article
- Evidence for the role of corticotropin-releasing factor in major depressive disorder.Neuroscience and biobehavioral reviews · 2015Review
- Treatment-resistant depression: are animal models of depression fit for purpose?Psychopharmacology · 2015Review
- Corticotropin-releasing hormone drives anandamide hydrolysis in the amygdala to promote anxiety.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Cell type-specific modifications of corticotropin-releasing factor (CRF) and its type 1 receptor (CRF1) on startle behavior and sensorimotor gating.Psychoneuroendocrinology · 2015Article
- An N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess.Endocrinology · 2014Article
- Behavioral Studies and Genetic Alterations in Corticotropin-Releasing Hormone (CRH) Neurocircuitry: Insights into Human Psychiatric Disorders.Behavioral sciences (Basel, Switzerland) · 2012Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The corticotropin-releasing hormone (CRH) and its cognate receptors have been implicated in the pathophysiology of stress-related disorders. Hypersecretion of central CRH and elevated glucocorticoid levels, as a consequence of impaired feedback control, have been shown to accompany mood and anxiety disorders. However, a clear discrimination of direct effects of centrally hypersecreted CRH from those resulting from HPA axis activation has been difficult. Applying a conditional strategy, we have generated two conditional CRH-overexpressing mouse lines: CRH-COE ( Del ) mice overexpress CRH throughout the body, while CRH-COE ( APit ) mice selectively overexpress CRH in the anterior and intermediate lobe of the pituitary. Both mouse lines show increased basal plasma corticosterone levels and consequently develop signs of Cushing's syndrome. However, while mice ubiquitously overexpressing CRH exhibited increased anxiety-related behaviour, overexpression of CRH in the pituitary did not produce alterations in emotional behaviour. These results suggest that chronic hypercorticosteroidism alone is not sufficient to alter anxiety-related behaviour but rather that central CRH hyperdrive on its own or in combination with elevated glucocorticoids is responsible for the increase in anxiety-related behaviour. In conclusion, the generated mouse lines represent valuable animal models to study the consequences of chronic CRH overproduction and HPA axis activation.
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