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Nitrous Oxide (N 2 O) Exposure Increases Neuronal Nitric Oxide Synthase (nNOS) Expression in Mouse Brain
Author(s) -
Zhang Yangmiao,
Koh David,
Quock Raymond
Publication year - 2013
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.27.1_supplement.654.21
Subject(s) - nitric oxide , nitric oxide synthase , chemistry , nitrous oxide , neuronal nitric oxide synthase , endocrinology , apoptosis , medicine , pharmacology , anesthesia , biochemistry
N 2 O has been known to possess an analgesic property since the late 18 th century. Since then, researchers have proposed different hypotheses for the mechanism, including an opioid/nitric oxide (NO) hypothesis (Emmanouil and Quock, Anesth Prog 54:9–18, 2007). Previously, we reported that N 2 O antinociception can be reduced by blocking NO production in the brain with selective nNOS inhibitor SMTC (Ishikawa and Quock, JPET 306:484–489, 2003). Recently, we found that increasing nNOS expression in brain contributes to HBO 2 antinociception (Zhang et al. , SfN Abstracts 38:575.29, 2012). The aim of this study was to discover whether N 2 O exposure also changes nNOS expression in the brain. Male NIH Swiss mice were exposed to 50% N 2 O for 60 min and sacrificed at intervals 0–8 hrs later. Brains were removed and divided into six coronal sections using a brain matrix. Expression of nNOS was examined by the western blotting assay. Results demonstrated that N 2 O treatment increased nNOS expression mostly in section 5 (−4.65 mm to −6.75 mm AP from bregma) and section 6 (−6.75 mm to −8.75 mm AP). The increase lasted for at least 8 hrs, which differs from HBO 2 ‐induced nNOS expression that peaked at 6 hr. Based on these findings, we conclude that N 2 O exposure increased nNOS expression in the caudal mouse brain. (This research was supported by NIH Grant AT‐007222 and the Allen I. White Distinguished Professorship at Washington State University.)