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Related Experiment Videos

RU486 blocks fasting-induced decrease of neuronal nitric oxide synthase in the rat paraventricular nucleus.

Yun Mi Kim1, Joo Young Lee, Si Ho Choi

  • 1Department of Pharmacology and BK 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, South Korea.

Brain Research
|July 28, 2004
PubMed
Summary

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Fasting reduces neuronal nitric oxide synthase (nNOS) in the brain's paraventricular nucleus (PVN). Glucocorticoids, stress hormones, mediate this reduction via the glucocorticoid receptor in the medial PVN.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Molecular Biology

Background:

  • Food deprivation is known to decrease neuronal nitric oxide synthase (nNOS) expression in the hypothalamic paraventricular nucleus (PVN).
  • Nitric oxide in the PVN is implicated in regulating autonomic functions, which are altered during food deprivation.
  • Elevated plasma glucocorticoids during fasting suggest a potential role in mediating nNOS down-regulation.

Purpose of the Study:

  • To investigate the molecular mechanism by which food deprivation decreases nNOS expression in the PVN.
  • To determine if plasma glucocorticoids mediate the fasting-induced down-regulation of PVN-nNOS.

Main Methods:

  • Male Sprague-Dawley rats were subjected to 48 hours of food deprivation.
  • Rats received either a vehicle or RU486 (glucocorticoid receptor antagonist) treatment.

Related Experiment Videos

  • Immunohistochemistry was used to assess nNOS and phosphorylated cAMP response element-binding protein (pCREB) immunoreactivity in PVN sections.

    • Main Results:

    • Food deprivation significantly decreased nNOS and pCREB immunoreactivity in the medial parvocellular PVN.
    • RU486 administration blocked the food deprivation-induced reduction of nNOS and pCREB in the medial parvocellular PVN.
    • In the posterior magnocellular PVN, food deprivation decreased nNOS immunoreactivity, but RU486 had no effect.

    Conclusions:

    • Glucocorticoid receptors likely mediate the fasting-induced down-regulation of nNOS in the parvocellular PVN.
    • This mechanism does not appear to apply to the magnocellular PVN.
    • Findings elucidate a molecular pathway linking fasting, glucocorticoids, and autonomic regulation via nNOS in the PVN.