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Cited by 217Stress Responses and CortisolNeuropeptides and Animal PhysiologyReceptor Mechanisms and Signaling

Role of CRF Receptor Signaling in Stress Vulnerability, Anxiety, and Depression

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Hauger, Richard L., Risbrough, Victoria, Oakley, Robert H., Olivares‐Reyes, J. Alberto, Dautzenberg, Frank M.·2009·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2009.05011.xPMC PMC3115623
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Abstract

Markers of hyperactive central corticotropin releasing factor (CRF) systems and CRF‐related single nucleotide polymorphisms (SNPs) have been identified in patients with anxiety and depressive disorders. Designing more effective antagonists may now be guided by data showing that small molecules bind to transmembrane domains. Specifically, CRF 1 receptor antagonists have been developed as novel anxiolytic and antidepressant treatments. Because CRF 1 receptors become rapidly desensitized by G protein‐coupled receptor kinase (GRK) and β‐arrestin mechanisms in the presence of high agonist concentrations, neuronal hypersecretion of synaptic CRF alone may be insufficient to account for excessive central CRF neurotransmission in stress‐induced affective pathophysiology. In addition to desensitizing receptor function, GRK phosphorylation and β‐arrestin binding can shift a G protein‐coupled receptor (GPCR) to signal selectively via the extracellular signal‐regulated kinase/mitogen‐activated protein kinase (ERK‐MAPK) or Akt pathways independent of G proteins. Also, Epac‐dependent CRF 1 receptor signaling via the ERK‐MAPK pathway has been found to potentiate brain‐derived neurotrophic factor (BDNF)‐stimulated TrkB signaling. Thus, genetic or acquired abnormalities in GRK and β‐arrestin function may be involved in the pathophysiology of stress‐induced anxiety and depression.

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  • In psychiatry, depression is conceptualized as heterogeneous, multifactorial in causation, and believed to arise from cumulative effects of genetics, adverse events in childhood, and ongoing life stressors.

    “Moreover, in psychiatry depression is conceptualized as heterogeneous, multifactorial in causation, and it is believed to arise from the cumulative effects [56–58] of genetics [59–62], adverse events in childhood [63–66], and ongoing life stressors [67–70].”

    From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [60]

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Authors
Hauger, R. L., Risbrough, V., Oakley, R. H., Olivares‐Reyes, J. A., & Dautzenberg, F. M.
Affiliations
  • University of California San Diego (US)
  • National Institutes of Health (US)
Corresponding author
Hauger, Richard L.
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2009-10
Volume
1179
Issue
1
Pages
120-143
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2009.05011.x
PMC
PMC3115623
OpenAlex
W2110748165
Cited by
217
References
11
Citations by year
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FWCI
0.84
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 33 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG022982)
  • National Institute of Mental Health (R01MH074697)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
corticotropin-releasing factor, CRF1 receptor, stress vulnerability, anxiety, depression, G protein-coupled receptor desensitization, beta-arrestin, ERK signaling, Epac, BDNF/TrkB signaling, CRF receptor antagonists, single nucleotide polymorphisms
MeSH terms
Anxiety, Anxiety Disorders, Depression, Humans, Hypothalamo-Hypophyseal System, Models, Biological, Pituitary-Adrenal System, Stress, Psychological, Signal Transduction, Receptors, Corticotropin-Releasing Hormone

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