Effects of beta-phenylethylamine on the hypothalamo-pituitary-adrenal axis in the male rat
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Updated: Aug 18, 2026

Combining Behavioral Endocrinology and Experimental Economics: Testosterone and Social Decision Making
Published on: March 2, 2011
E Kosa1, A Marcilhac-Flouriot, M P Fache
1Laboratoire des Interactions Fonctionnelles en Neuroendocrinologie, U-501 INSERM, Faculté de Médecine de Marseille-Nord, Boulevard Pierre Dramard, 13916 Cedex 20, Marseille, France.
Abstract:
beta-Phenylethylamine (PEA) is a trace neuroactive amine implicated in the regulation of the hypothalamic-pituitary-adrenal (HPA) response to stress. To test this hypothesis, effects of subchronic levels of PEA (50 mg/kg/day treatment for 10 days) on the corticotroph function were studied. PEA treatment induces: (i) a significant increase of corticotrophin releasing hormone (CRH) immunoreactivity in the median eminence (ME), as measured by semi-quantitative immunofluorescence labeling techniques, (ii) a significant increase in CRH mRNA levels in paraventricular nuclei, as detected by in situ hybridization, and (iii) an increase in plasma adreno-corticotrophin hormone (ACTH) and corticosterone levels in responses to stress. PEA treatment has no effect on the number of binding sites and on the dissociation constant of the glucocorticoid receptors in any structure studied. Results of the dexamethasone suppression test were similar in PEA- and saline-treated rats. Taken together, these results suggest that PEA treatment stimulated the HPA axis activity levels directly via the CRH hypothalamic neurons, without altering the negative feed back control exerted by the glucocorticoids.
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