Role of Nitric Oxide in Alcohol Alteration of β-Endorphin Release from Hypothalamic Cells in Primary Cultures

Nadka I. Boyadjieva, Cui P. Chen, Dipak K. Sarkar

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Background: Nitric oxide (NO) mediates many pharmacological actions of ethanol. NO's role in regulating ethanol action on hypothalamic β-endorphin (β-EP) neurons is not established. Methods: In this study, we determined the role of NO in ethanol regulation of β-EP release from primary cultures of rat fetal mediobasal hypothalamic cells. Real-time polymerase chain reaction was used for messenger RNA (mRNA) detection; radioimmunoassay was used for hormone measurements. Results: Acute ethanol treatment for 3 hr increased the release of β-EP but reduced nitrite levels in the media of hypothalamic cells in primary cultures. In contrast, ethanol exposure for 48 hr reduced the release of β-EP but increased the release of nitrite from these cells. Alcohol treatments altered the expression of neuronal NO synthase mRNA, but not inducible NO synthase mRNA, in a pattern similar to that of nitrite levels. Alcohol treatments blocked sodium nitroprusside-induced increases in the level of cellular cyclic guanidine monophosphate. The nonspecific NO blocker N G-nitro-L-arginine-methyl-esther, but not the inactive isomer N-nitro-D-arginine-methyl-esther (D-NAME), inhibited ethanol inhibitory actions on β-EP release. Conclusions: These results suggest that the cyclic guanidine monophosphate/NO pathway is involved in ethanol alteration of hypothalamic β-EP release.

Original languageAmerican English
Pages (from-to)1813-1818
Number of pages6
JournalAlcoholism: Clinical and Experimental Research
Issue number11
StatePublished - Nov 2003

ASJC Scopus subject areas

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


  • Ethanol
  • Gene Expression
  • Inducible Nitric Oxide Synthase (iNOS)
  • Neuronal Nitric Oxide Synthase (nNOS)
  • β-Endorphin Neurons


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