ReviewFrontiers in neuroscience2013
Corticotropin-releasing factor-related peptides, serotonergic systems, and emotional behavior.
Review in Frontiers in neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 102 citations in OpenAlex.
- High-fat diet, microbiome-gut-brain axis signaling, and anxiety-like behavior in male rats.Biological research · 2024Article
- The role of brain serotonin signaling in excessive alcohol consumption and withdrawal: A call for more research in females.Neurobiology of stress · 2024Article
- RareHeliyon · 2024Article
- Corticotropin-Releasing Hormone: A Novel Stimulator of Somatolactin in Teleost Pituitary Cells.Cells · 2023Article
- Organization of the corticotropin-releasing hormone and corticotropin-releasing hormone-binding protein systems in the central nervous system of the sea lamprey Petromyzon marinus.The Journal of comparative neurology · 2023Article
- Alterations of Gut-Derived Melatonin in Neurobehavioral Impairments Caused by Zinc Oxide Nanoparticles.International journal of nanomedicine · 2023Article
- Corticotropin releasing factor and drug seeking in substance use disorders: Preclinical evidence and translational limitations.Addiction neuroscience · 2022Article
- Receptor-Mediated AKT/PI3K Signalling and Behavioural Alterations in Zebrafish Larvae Reveal Association between Schizophrenia and Opioid Use Disorder.International journal of molecular sciences · 2022Article
- Sex-Related Predisposition to Post-Traumatic Stress Disorder Development-The Role of Neuropeptides.International journal of environmental research and public health · 2021Review
- Interaction between intensity and duration of acute exercise on neuronal activity associated with depression-related behavior in rats.The journal of physiological sciences : JPS · 2021Article
- CRF-5-HT interactions in the dorsal raphe nucleus and motivation for stress-induced opioid reinstatement.Psychopharmacology · 2021Article
- Neuromodulation and Behavioral Flexibility in Larval Zebrafish: From Neurotransmitters to Circuits.Frontiers in molecular neuroscience · 2021Article
- Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation.Brain sciences · 2020Review
- Agonist bias and agonist-dependent antagonism at corticotrophin releasing factor receptors.Pharmacology research & perspectives · 2020Article
- Diet and Mental Health: Review of the Recent Updates on Molecular Mechanisms.Antioxidants (Basel, Switzerland) · 2020Review
- Corticotropin-Releasing Hormone (CRH) Gene Family Duplications in Lampreys Correlate With Two Early Vertebrate Genome Doublings.Frontiers in neuroscience · 2020Article
- Effects of maternal separation on serotonergic systems in the dorsal and median raphe nuclei of adult male Tph2-deficient mice.Behavioural brain research · 2019Article
- The dynamic serotonin system of the maternal brain.Archives of women's mental health · 2019Article
- Mitochondria: A Connecting Link in the Major Depressive Disorder Jigsaw.Current neuropharmacology · 2019Review
- Negative consequences of early-life adversity on substance use as mediated by corticotropin-releasing factor modulation of serotonin activity.Neurobiology of stress · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Corticotropin-releasing factor (CRF) is a 41-amino acid neuropeptide that is involved in stress-related physiology and behavior, including control of the hypothalamic-pituitary-adrenal (HPA) axis. Members of the CRF family of neuropeptides, including urocortin 1 (UCN 1), UCN 2, and UCN 3, bind to the G protein-coupled receptors, CRF type 1 (CRF1) and CRF2 receptors. In addition, CRF binding protein (CRFBP) binds both CRF and UCN 1 and can modulate their activities. There are multiple mechanisms through which CRF-related peptides may influence emotional behavior, one of which is through altering the activity of brainstem neuromodulatory systems, including serotonergic systems. CRF and CRF-related peptides act within the dorsal raphe nucleus (DR), the major source for serotonin (5-HT) in the brain, to alter the neuronal activity of specific subsets of serotonergic neurons and to influence stress-related behavior. CRF-containing axonal fibers innervate the DR in a topographically organized manner, which may contribute to the ability of CRF to alter the activity of specific subsets of serotonergic neurons. CRF and CRF-related peptides can either increase or decrease serotonergic neuronal firing rates and serotonin release, depending on their concentrations and on the specific CRF receptor subtype(s) involved. This review aims to describe the interactions between CRF-related peptides and serotonergic systems, the consequences for stress-related behavior, and implications for vulnerability to anxiety and affective disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.