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.
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.
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.
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.
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.
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.
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.
Dysfunction of the CRF system has been observed in stress-related affective disorders including post-traumatic stress disorder, depression, and anxiety.
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.
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-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 binds with high affinity to CRF receptor 1 (CRFR1) and is implicated in stress-related mood disorders such as anxiety and depression.
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.