Activation of Brain Somatostatin Signaling Suppresses CRF Receptor-Mediated Stress Response.
| Autor: | Stengel A; Division of Psychosomatic Medicine, Charité Center for Internal Medicine and Dermatology, Charité-Universitätsmedizin BerlinBerlin, Germany., Taché YF; Vatche and Tamar Manoukian Digestive Diseases Division, CURE Digestive Diseases Research Center, G Oppenheimer Center for Neurobiology of Stress and Resilience, Department of Medicine, University of California, Los AngelesLos Angeles, CA, USA.; VA Greater Los Angeles Health Care SystemLos Angeles, CA, USA. |
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| Jazyk: | angličtina |
| Zdroj: | Frontiers in neuroscience [Front Neurosci] 2017 Apr 25; Vol. 11, pp. 231. Date of Electronic Publication: 2017 Apr 25 (Print Publication: 2017). |
| DOI: | 10.3389/fnins.2017.00231 |
| Abstrakt: | Corticotropin-releasing factor (CRF) is the hallmark brain peptide triggering the response to stress and mediates-in addition to the stimulation of the hypothalamus-pituitary-adrenal (HPA) axis-other hormonal, behavioral, autonomic and visceral components. Earlier reports indicate that somatostatin-28 injected intracerebroventricularly counteracts the acute stress-induced ACTH and catecholamine release. Mounting evidence now supports that activation of brain somatostatin signaling exerts a broader anti-stress effect by blunting the endocrine, autonomic, behavioral (with a focus on food intake) and visceral gastrointestinal motor responses through the involvement of distinct somatostatin receptor subtypes. |
| Databáze: | MEDLINE |
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