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Stress, Corticotrophin-Releasing Factor (CRF) and Gastric Function

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Neuroendocrinology of Gastrointestinal Ulceration

Part of the book series: Hans Selye Symposia on Neuroendocrinology and Stress ((HSSN,volume 2))

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Abstract

Selye1 demonstrated that many different kinds of “stressors” were associated with the development of gastric erosions (GE’s) in the rat. Since that time the number of methods for producing GE’s in the rat has grown exponentially2–4. Initially, the burden of the pathogenesis of GE was placed on the corticosteroids and on increases in gastric acid secretion (GAS). Yet, Cannon in 1929 first showed that GAS was reduced in the threatened cat. Since that time many different (stressful) perturbations of a physical and psychobiological nature have been shown to reduce GAS (reviewed in 5): They include restraining or rotating rats, exposing them to unpredictable electric shock or making them avoid it in free-operant experiments, confronting them with an aggressive opponent, or housing them in a hot environment.

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Authors
  1. Herbert Weiner
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Editors and Affiliations

  1. Harvard Medical School, Boston, Massachusetts, USA

    Sandor Szabo

  2. Irvine VA Medical Center, University of California, Long Beach, California, USA

    Sandor Szabo

  3. Center for Ulcer Research and Education, University of California, Los Angeles, California, USA

    Yvette Taché

  4. University of Manitoba, Winnipeg, Manitoba, Canada

    Gary B. Glavin

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Weiner, H. (1995). Stress, Corticotrophin-Releasing Factor (CRF) and Gastric Function. In: Szabo, S., Taché, Y., Glavin, G.B. (eds) Neuroendocrinology of Gastrointestinal Ulceration. Hans Selye Symposia on Neuroendocrinology and Stress, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1867-9_13

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