Year: 2003
Type: dissertation
Abstract: The mechanism of the clinical anxiolytic effect of nitrous oxide (N 2 O) remains incompletely understood.We have hypothesized that N 2 O stimulates the benzodiazepine (BZ)/γ-aminobutyric acid A (GABA A ) receptor complex, which activates a signaling pathway involving nitric oxide (NO) and cyclic GMP (cGMP).This hypothesis was tested through a series of studies in the mouse light/dark exploration test.The first study compared the anxiolytic-like behavioral effects of N 2 O and chlordiazepoxide following BZ and GABA A receptor blockade and nitric oxide synthase (NOS) inhibition.Based on these findings, we conclude that the pathway activated by N 2 O and chlordiazepoxide involves BZ and GABA A receptors as well as NO.The second study demonstrated further the involvement of NO by assessing the influence of N 2 O on brain NOS activity and utilizing an NO scavenger as well as selective inhibitors of the three isoforms of NOS.Based on these findings, we conclude that NO is a *
Author: Shuang Li
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
Funder: National Institutes of Health
OpenAlex ID: W2117568519