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Review
. 2017 Apr 25:11:231.
doi: 10.3389/fnins.2017.00231. eCollection 2017.

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

Andreas Stengel  1 , Yvette F Taché  2   3
Affiliations
Review

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

Andreas Stengel et al. Front Neurosci. .

Abstract

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.

Keywords: HPA; brain-gut axis; food intake; gastrointestinal functions; hypothalamus; stress.

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Figures

Figure 1
Figure 1
Brain interaction of CRF and somatostatin signaling. Stress activates the hypothalamus-pituitary-adrenal gland axis by stimulating the hormones corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH) and corticosterone. This stimulation is modulated by somatostatin signaling via different somatostatin receptors (sst). Green arrows indicate a stimulatory effect, red arrows depict an inhibition.
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