The most robustly confirmed neuroendocrine finding among psychiatric patients with affective disorders is hyperactivity of the hypothalamic-pituitary-adrenocortical (HPA) system, resulting from hyperactive hypothalamic corticotropin-releasing hormone (CRH) neurons.
Given the fundamental role of the corticotropin-releasing hormone (CRH) system in anxiety, stress-associated pathologies, and mood disorders, we describe genetic modifications of the genes that encode proteins integral to the CRH/CRH receptor system with particular emphasis on conditional gene-targeting strategies.
We conclude that androgens may directly affect CRH neurons in the human PVN via AR binding to the CRH-ARE, which may have consequences for sex-specific pathogenesis of mood disorders.
Dysfunctioning of corticotropin-releasing factor (CRF) and its receptors (CRF(1) and CRF(2)) has been linked to the development of stress-related disorders, such as affective disorders and drug abuse.
Corticotropin-releasing factor-binding protein (CRF-BP) regulates the availability of free CRF and is a functional candidate gene for affective disorders.
Corticotropin-releasing factor-binding protein (CRF-BP) regulates the availability of free CRF and is a functional candidate gene for affective disorders.
Corticotropin-releasing factor-binding protein regulates the availability of free corticotropin-releasing factor and is a functional candidate gene for affective disorders.
Corticotropin-releasing factor-binding protein regulates the availability of free corticotropin-releasing factor and is a functional candidate gene for affective disorders.
Corticotropin-releasing factor (CRF), its receptors, and signaling pathways that regulate CRF expression and responses are areas of intense investigation for new drugs to treat affective disorders.
The density of RAR-alpha-immunoreactive neurons and CRH-RAR-alpha double-staining neurons was significantly increased in the PVN of patients with affective disorders.
These results indicate that the central CRF signal, rather than the peripheral CRF signal would be related to anxiety and other behavioral changes, and CRF<sub>1</sub> receptor antagonism in the central nervous system may be critical for identifying drug candidates for anxiety and mood disorders.
Decades of research have described the importance of corticotropin-releasing factor (CRF) signaling in alcohol addiction, as well as in commonly co-expressed neuropsychiatric diseases, including anxiety and mood disorders.
These findings show that stress activates BNST CRF neurons, and that α<sub>2A</sub>-AR activation suppresses the <i>in vivo</i> activity of these cells, at least in part by suppressing excitatory drive from PBN inputs onto CRF neurons.<b>SIGNIFICANCE STATEMENT</b> Stress is a major variable contributing to mood disorders.
Corticotropin-releasing factor binds with high affinity to CRF receptor 1 (CRFR1) and is implicated in stress-related mood disorders such as anxiety and depression.
Dysfunction of the CRF system has been observed in stress-related affective disorders including post-traumatic stress disorder, depression, and anxiety.