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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: Gastroenterology. 2009 Oct 1;138(1):294. doi: 10.1053/j.gastro.2009.09.054

Figure 8.

Figure 8

A schematic illustrating the proposed mechanism of HeCS-induced visceral hypersensitivity to CRD in relation to the well-established elements of the stress response. Step 1: Stress releases of CRH and angiotensin vasopressin from the paraventricular nucleus in the hypothalamus. CRH releases adrenocorticotropic hormone and other mediators from the pituitary. Step 2. CRH and arginine vasopressin stimulate the locus ceruleus/norepinephrine system. Step 3. The activation of the sympathetic preganglionic neurons releases norepinephrine/epinephrine in blood stream from the adrenal medulla. Step 4: Norepinephrine elevates the expression of NGF in colonic muscularis externa and mucosa/submucosa. Step 5: NGF complexes with trkA receptors and the complex transports retrograde to the thoracolumbar DRG. Step 6: NGF/trkA complex sensitizes colon-specific neurons by modulating the expression and characteristics of ion channels Step 7: The amplification of afferent signal in response to CRD is perceived as abdominal pain/discomfort.