Elsevier

Brain Research Bulletin

Volume 17, Issue 3, September 1986, Pages 285-289
Brain Research Bulletin

Article
CRF antagonist partially reverses CRF- and stress-induced effects on feeding

https://doi.org/10.1016/0361-9230(86)90233-9Get rights and content

Abstract

Exogenous corticotropin releasing factor (CRF) causes centrally mediated behavioral changes including decreased feeding and increased grooming. These behavioral changes are also seen in response to some stressors. However, the role of endogenous CRF in the behavioral response to stressors has not been investigated fully. We report below our findings on the behavioral effects of alpha-helical CRF (9–41), a recently discovered competitive antagonist of CRF-induced ACTH release. Alpha-helical CRF (9–41) partially reversed the decrement in feeding induced by CRF. Furthermore, the reduction in food intake due to restraint stress was partially reversed by alpha-helical CRF (9–41). These results indicate that changes in endogenous CRF release induced by the restraint Stressor may play a role in stress-induced anorexia.

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  • Hypothalamic mechanisms associated with corticotropin-releasing factor-induced anorexia in chicks

    2019, Neuropeptides
    Citation Excerpt :

    The CRF antagonist, α-helical CRF, attenuated the anorectic effects of CRF injection into the PVN but not other hypothalamic nuclei such as the ventromedial hypothalamus (VMH) (Kalra et al. 1999). Additionally, central injection of α-helical CRF augments NPY-induced hunger (Heinrichs et al. 1992), and blunts the reduction in food intake caused in response to restraint (Krahn et al. 1986) and tail pinch (Heinrichs et al. 1992) stress and exercise (Rivest and Richard 1990), which suggests that endogenous CRF plays a physiological role in appetite regulation. This is consistent with observations that endogenous CRF production is affected by a variety of factors that affect feeding behavior, including drugs such as fenfluramine (Appel et al. 1991), obesity (Richard et al. 1996), and tumor-induced anorexia (McCarthy et al. 1993).

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