In the past, Acetaldehyde (ACD), the main metabolite of ethanol (ETOH), was mainly studied for its toxic and adverse effects (1). However, recently, ACD was reported to determine behavioural and neurochemical effects, following ETOH assumption in rodents (2, 3). Indeed, ACD enhances dopamine levels in nucleus accumbens, stimulates beta-endorphin release from hypothalamic cells, mediating alcohol reinforcing effects (4). Since little is known about the effects of ACD on other central neuropeptides, in this research we aimed to investigate ACD influence on hypothalamic corticotropin-releasing factor (CRF) release.In order to ascertain this hypothesis, different doses of ACD (1, 10, 3x10 microM) have been administered in incubated hypothalamic explants and CRF concentration have been detected by a radioimmunoassay. Our results show that, following 20 min of incubation at 37°C, ACD is able to significantly increase hypothalamic CRF release in a dose-dependent manner (p<0.05). This effect could be exerted by ACD itself or by other mediators; anyway this could explain the well-known stimulating effect induced by EtOH on ACTH release (5). Further experiments are needed to clarify the mechanisms underlying ACD effect on central neurotransmission.1. Glud. E. Q J Stud Alcohol. 1949 Sep; 10(2):185-97.2. Webb et all. Alcohol Clin Exp Res. 2002 May; 26(5):695-7043. Zimatkin et all Alcohol Clin Exp Res. 2001 Jul; 25(7):982-8.4. Rodd-Henrichs et al Pharmacol Biochem Behav 72 (1-2):55 645. Lee S. et all Endocrinology 145 (10): 4470- 4479.
|Numero di pagine||1|
|Stato di pubblicazione||Published - 2008|