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Central apelin contributes to stress‐induced impaired gastric motility in rats
Author(s) -
Bülbül Mehmet,
Uysal Nimet,
Birsen Ilknur,
Gemici Burcu,
Tanriöver Gamze
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb791
Subject(s) - apelin , endocrinology , medicine , stressor , hypothalamus , microdialysis , downregulation and upregulation , corticotropin releasing hormone , antagonist , receptor , central nervous system , chemistry , clinical psychology , biochemistry , gene
Stress plays a major role in functional gastrointestinal (GI) disorders. GI symptoms may develop as a result of accumulation stressors in some individuals while others can adapt to stressors. Exposure to repeated experience with the same stressor can produce an adaptation of behavioral and hypothalamic‐pituitary‐adrenal (HPA) axis response. However, the adaptation mechanism remains unclear. Acute restraint stress (ARS) increases corticotrophin releasing factor (CRF) in hypothalamic paraventricular nucleus (PVN) leads delayed gastric emptying (GE) via autonomic neural pathways in rats. ARS‐induced delayed GE is completely restored following chronic single stress (CSS) while restoration is no longer observed following chronic complicated stress (CCS). Apelin is upregulated in PVN in response to stress. Central effects of apelinergic system are attributed to regulation of stress response. We performed GE measurement and brain microdialysis from PVN under non‐stressed, ARS, CSS and CCS conditions in rats. ARS significantly increased CRF and apelin concentrations. CSS attenuated this response, whilst concentrations remained significantly high following CCS. ARS delayed GE which was completely restored following CSS, but not CCS. Central administration of apelin antagonist F13A restored delayed GE following ARS and CCS. Thus, apelin may be a candidate for treatment of stress‐induced GI disorders.