Ethanol Modulates Corticotropin Releasing Hormone Release From the Rat Hypothalamus: Does Acetaldehyde Play a Role?

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Abstract

Background and Methods: Ethanol (EtOH)activates hypothalamic–pituitary–adrenal(HPA) axis, resulting in adrenocorticotropin hormone, glucocorticoid release, and in modifications of the response of the axis to other stressors. The initial site of EtOH action within the HPA system seems to be the hypothalamus. Thus, to determine the mechanisms responsible for these effects, we investigated: (i) whether EtOH was able to release corticotrophic releasing hormone (CRH)from incubated hypothalamic explants; (ii) whether acetaldehyde (ACD), its first metabolite formed in the brain by catalase activity, might play a role in EtOH activity. To this aim, rat hypothalamic explants were incubated with: (i) medium containing EtOH at 32.6 · 103 lM; (ii) different concentration of ACD (1, 3, 10, and 30 lM); (iii) EtOH plus 3amino-1,2,4-triazole (3AT, 32 · 103 lM) an inhibitor of cerebral catalase; (iv) ACD plus D-penicillamine (DP, 50.3 · 103 lM) an ACD-trapping agent. CRH levels were evaluated by a radioimmunoassay. Results: Incubation with EtOH induced a 7-fold increase in CRH secretion, with respect to basal levels; ACD was able to stimulate CRH release in a dose-dependent manner; the inhibition of cerebral catalase by 3AT blocked EtOH-induced CRH outflow; the inactivation of ACD by DP reverted the ACD-stimulating effect on CRH secretion. Conclusions: These data show that both EtOH and acetaldehyde are able to increase hypothalamic CRH release from the rat hypothalamus and that acetaldehyde itself appears to be the mediator of EtOH activity.
Lingua originaleEnglish
pagine (da-a)588-593
Numero di pagine6
RivistaALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
Volume34
Stato di pubblicazionePublished - 2010

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Acetaldehyde
Corticotropin-Releasing Hormone
Hypothalamus
Rats
Ethanol
Hormones
Catalase
Pituitary Hormone-Releasing Hormones
Pituitary-Adrenal System
Penicillamine
Metabolites
Adrenocorticotropic Hormone
Glucocorticoids
Radioimmunoassay
Brain

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Psychiatry and Mental health
  • Toxicology

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@article{f6bb7c60890843eaa1e80bb52e32d7e1,
title = "Ethanol Modulates Corticotropin Releasing Hormone Release From the Rat Hypothalamus: Does Acetaldehyde Play a Role?",
abstract = "Background and Methods: Ethanol (EtOH)activates hypothalamic–pituitary–adrenal(HPA) axis, resulting in adrenocorticotropin hormone, glucocorticoid release, and in modifications of the response of the axis to other stressors. The initial site of EtOH action within the HPA system seems to be the hypothalamus. Thus, to determine the mechanisms responsible for these effects, we investigated: (i) whether EtOH was able to release corticotrophic releasing hormone (CRH)from incubated hypothalamic explants; (ii) whether acetaldehyde (ACD), its first metabolite formed in the brain by catalase activity, might play a role in EtOH activity. To this aim, rat hypothalamic explants were incubated with: (i) medium containing EtOH at 32.6 · 103 lM; (ii) different concentration of ACD (1, 3, 10, and 30 lM); (iii) EtOH plus 3amino-1,2,4-triazole (3AT, 32 · 103 lM) an inhibitor of cerebral catalase; (iv) ACD plus D-penicillamine (DP, 50.3 · 103 lM) an ACD-trapping agent. CRH levels were evaluated by a radioimmunoassay. Results: Incubation with EtOH induced a 7-fold increase in CRH secretion, with respect to basal levels; ACD was able to stimulate CRH release in a dose-dependent manner; the inhibition of cerebral catalase by 3AT blocked EtOH-induced CRH outflow; the inactivation of ACD by DP reverted the ACD-stimulating effect on CRH secretion. Conclusions: These data show that both EtOH and acetaldehyde are able to increase hypothalamic CRH release from the rat hypothalamus and that acetaldehyde itself appears to be the mediator of EtOH activity.",
author = "Carla Cannizzaro and Fulvio Plescia and Silvana Cacace and {La Barbera}, Marco and Giuseppe Tringali",
year = "2010",
language = "English",
volume = "34",
pages = "588--593",
journal = "Alcoholism: Clinical and Experimental Research",
issn = "0145-6008",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Ethanol Modulates Corticotropin Releasing Hormone Release From the Rat Hypothalamus: Does Acetaldehyde Play a Role?

AU - Cannizzaro, Carla

AU - Plescia, Fulvio

AU - Cacace, Silvana

AU - La Barbera, Marco

AU - Tringali, Giuseppe

PY - 2010

Y1 - 2010

N2 - Background and Methods: Ethanol (EtOH)activates hypothalamic–pituitary–adrenal(HPA) axis, resulting in adrenocorticotropin hormone, glucocorticoid release, and in modifications of the response of the axis to other stressors. The initial site of EtOH action within the HPA system seems to be the hypothalamus. Thus, to determine the mechanisms responsible for these effects, we investigated: (i) whether EtOH was able to release corticotrophic releasing hormone (CRH)from incubated hypothalamic explants; (ii) whether acetaldehyde (ACD), its first metabolite formed in the brain by catalase activity, might play a role in EtOH activity. To this aim, rat hypothalamic explants were incubated with: (i) medium containing EtOH at 32.6 · 103 lM; (ii) different concentration of ACD (1, 3, 10, and 30 lM); (iii) EtOH plus 3amino-1,2,4-triazole (3AT, 32 · 103 lM) an inhibitor of cerebral catalase; (iv) ACD plus D-penicillamine (DP, 50.3 · 103 lM) an ACD-trapping agent. CRH levels were evaluated by a radioimmunoassay. Results: Incubation with EtOH induced a 7-fold increase in CRH secretion, with respect to basal levels; ACD was able to stimulate CRH release in a dose-dependent manner; the inhibition of cerebral catalase by 3AT blocked EtOH-induced CRH outflow; the inactivation of ACD by DP reverted the ACD-stimulating effect on CRH secretion. Conclusions: These data show that both EtOH and acetaldehyde are able to increase hypothalamic CRH release from the rat hypothalamus and that acetaldehyde itself appears to be the mediator of EtOH activity.

AB - Background and Methods: Ethanol (EtOH)activates hypothalamic–pituitary–adrenal(HPA) axis, resulting in adrenocorticotropin hormone, glucocorticoid release, and in modifications of the response of the axis to other stressors. The initial site of EtOH action within the HPA system seems to be the hypothalamus. Thus, to determine the mechanisms responsible for these effects, we investigated: (i) whether EtOH was able to release corticotrophic releasing hormone (CRH)from incubated hypothalamic explants; (ii) whether acetaldehyde (ACD), its first metabolite formed in the brain by catalase activity, might play a role in EtOH activity. To this aim, rat hypothalamic explants were incubated with: (i) medium containing EtOH at 32.6 · 103 lM; (ii) different concentration of ACD (1, 3, 10, and 30 lM); (iii) EtOH plus 3amino-1,2,4-triazole (3AT, 32 · 103 lM) an inhibitor of cerebral catalase; (iv) ACD plus D-penicillamine (DP, 50.3 · 103 lM) an ACD-trapping agent. CRH levels were evaluated by a radioimmunoassay. Results: Incubation with EtOH induced a 7-fold increase in CRH secretion, with respect to basal levels; ACD was able to stimulate CRH release in a dose-dependent manner; the inhibition of cerebral catalase by 3AT blocked EtOH-induced CRH outflow; the inactivation of ACD by DP reverted the ACD-stimulating effect on CRH secretion. Conclusions: These data show that both EtOH and acetaldehyde are able to increase hypothalamic CRH release from the rat hypothalamus and that acetaldehyde itself appears to be the mediator of EtOH activity.

UR - http://hdl.handle.net/10447/49307

M3 - Article

VL - 34

SP - 588

EP - 593

JO - Alcoholism: Clinical and Experimental Research

JF - Alcoholism: Clinical and Experimental Research

SN - 0145-6008

ER -