ABSTRACT

The G protein-coupled receptor CRF1 plays a crucial part in the stress reaction and is mainly expressed in the brain. “Corticotropin-releasing factor” (CRF), which the brain secretes in reaction to stress, activates the receptor. When CRF binds to the CRF1 receptor, it causes the pituitary gland to produce adrenocorticotropic hormone (ACTH), which then causes the adrenal glands to generate stress hormones like cortisol. The CRF1 receptor regulates behaviours associated with depression, anxiety, and addiction in addition to stress reaction. Depression, anxiety, and post-traumatic stress disorder are just a few of the mental and stress- related conditions the brain experiences when the CRF1 receptor isn't functioning properly (PTSD). The CRF1 receptor has been thoroughly investigated for possible therapeutic uses in the therapy of stress-related illnesses as a potential pharmacological target. The impacts of CRF1 receptor antagonists (CRAs) are detected by anxiolytics and/or antidepressants in a number of animal stress models, and their possible therapeutic value in the management of “depression, anxiety, and other stress-related diseases is assessed”. By inhibiting pituitary and possibly brain CRF1 receptors, CRAs lessen the HPA axis activation brought on by stresses, which may lessen the sickness brought on by prolonged stress. For the therapy of melancholy, anxiety, and PTSD, several CRF1 receptor antagonists have been created and are presentlyundergoing clinical studies. The effectiveness of these substances is still being researched, though. This overview emphasises the CRF1 receptor's therapeutic value, which is an area of active study and holds great potential for the creation of innovative therapies for disorders linked to stress. Keyword: Corticotrophin releasing factor type 1 (CRF-1), ACTH, Depression, Anxiety
Publication date: 01/04/2024

https://ijbpas.com/pdf/2024/April/MS_IJBPAS_2024_7970.pdf

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https://doi.org/10.31032/IJBPAS/2024/13.4.7970