Activation of Brain Somatostatin Signaling Suppresses CRF Receptor-Mediated Stress Response

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Andreas Stengel ; Yvette F. Taché ; Yvette F. Taché (2017)
  • Publisher: Frontiers Media S.A.
  • Journal: Frontiers in Neuroscience (issn: 1662-453X)
  • Related identifiers: doi: 10.3389/fnins.2017.00231, doi: 10.3389/fnins.2017.00231/full
  • Subject: stress | Neurosciences. Biological psychiatry. Neuropsychiatry | gastrointestinal functions | RC321-571 | HPA | brain-gut axis | hypothalamus | food intake
    mesheuropmc: endocrine system | hormones, hormone substitutes, and hormone antagonists

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.
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