Ethanol releases corticotropic releasing hormone (CRH) from rat hypothalamic explants; role of acetaldehyde

Carla Cannizzaro, Fulvio Plescia, Marco La Barbera, Silvana Cacace

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Ethanol activates hypothalamic-pituitary-adrenal (HPA) axis, resulting in adrenocorticotropic hormone (ACTH) glucocorticoid release, and a modification of the response of this axis to other stressors (Lee et al 1999, 2000). To determine the mechanisms responsible for these effects we investigated : 1) whether ethanol was able to release CRH from incubated hypothalamic explants; 2) whether acetaldehyde (ACD), its first metabolite formed in the brain by catalase activity, might play a role in ethanol effects. To this aim, rat hypothalamic explants were incubated with: 1) medium containing ethanol at 150 mg %; 2) different concentrations of ACD (4.4, 13.2, 44, 132 x 10-3 mg%); 3) ethanol plus 3-amino-1,2,4-triazole (3-AT, 269 mg%), an inhibitor of cerebral catalase; 4) ACD plus D-penicillamine (D-P, 74.6 mg%), an ACD-trapping agent. CRH levels were evaluated by a radioimmunoassay. Our results show that: incubation with ethanol (150 mg %) induced a seven-fold increase in CRH secretion (p< 0.01); ACD was able to increase CRH release in a dose dependent manner (p<0.05; p<0.005); the inhibition of cerebral catalase by 3-AT blocked the ethanol-induced CRH outflow (p<0.01); the inactivation of ACD by D-P reverted the ACD-stimulating effect on CRH secretion (p<0.05). These data show that both ethanol and ACD are able to increase hypothalamic CRH release, and that ACD itself appears to be the mediator of ethanol activity.
Original languageEnglish
Number of pages1
Publication statusPublished - 2009

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