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 trea
tment induces: (i) a significant increase of corticotrophin releasing hormo
ne (CRH) immunoreactivity in the median eminence (ME), as measured by semi-
quantitative immunofluorescence labeling techniques, (ii) a significant inc
rease in CRH mRNA levels in paraventricular nuclei, as detected by in situ
hybridization, and (iii) an increase in plasma adreno-corticotrophin hormon
e (ACTH) and corticosterone levels in responses to stress. PEA treatment ha
s no effect on the number of binding sites and on the dissociation constant
of the glucocorticoid receptors in any structure studied. Results of the d
examethasone suppression test were similar in PEA- and saline-treated rats.
Taken together, these results suggest that PEA treatment stimulated the HP
A axis activity levels directly via the CRH hypothalamic neurons, without a
ltering the negative feed back control exerted by the glucocorticoids. (C)
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