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Nitrous oxide (N 2 O)‐induced nitric oxide (NO)‐dependent release of β‐endorphin (β‐EP) from the arcuate nucleus to stimulate opioid receptors in the periaqueductal gray (PAG) to cause antinociception in the rat
Author(s) -
Ohgami Yusuke,
Chung Eunhee,
Quock Raymond M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.711.15
Subject(s) - periaqueductal gray , chemistry , microinjection , opioid , microdialysis , endocrinology , medicine , nucleus , arcuate nucleus , pharmacology , hypothalamus , receptor , central nervous system , neuroscience , biology , biochemistry , midbrain
N 2 O stimulates an NO‐dependent release of endogenous opioid peptides to induced antinociception in rodents (Emmanouil & Quock, Anesth. Prog. 54:9–18, 2007). The present study was carried out to determine whether the arcuate nucleus was the brain site of action of N 2 O. Male Sprague Dawley rats, 250–300 g, were stereotaxically implanted with microdialysis probes in the arcuate nucleus. Exposure to 70% N 2 O increased dialysate levels of NO x as well as β‐EP, compared to levels in fractions collected under room air. Pretreatment of rats with the NOS‐inhibitor L‐NAME prior to N 2 O exposure antagonized the increases in both NO metabolites and β‐EP. In other rats that were stereotaxically implanted with intracerebral microinjection cannulae, pretreatment with naltrexone in the periaqueductal gray (PAG) but not the arcuate nucleus antagonized N 2 O‐induced antinociception in the rat hot plate test. These findings indicate a functional link between increased NO activity and neuronal release of β‐EP in response to N 2 O and support our hypothesis that β‐EP released from the arcuate nucleus is carried to the PAG to cause antinociception. (Supported by State of Washington Initiative Measure No. 171.)