ALTERATIONS IN CATECHOLAMINE TURNOVER IN SPECIFIC REGIONS OF THE RAT-BRAIN FOLLOWING ACUTE EXPOSURE TO NITROUS-OXIDE

Citation
Ar. Karuri et al., ALTERATIONS IN CATECHOLAMINE TURNOVER IN SPECIFIC REGIONS OF THE RAT-BRAIN FOLLOWING ACUTE EXPOSURE TO NITROUS-OXIDE, Brain research bulletin, 45(6), 1998, pp. 557-561
Citations number
32
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03619230
Volume
45
Issue
6
Year of publication
1998
Pages
557 - 561
Database
ISI
SICI code
0361-9230(1998)45:6<557:AICTIS>2.0.ZU;2-3
Abstract
The effects of nitrous oxide (N2O) on steady-state concentrations and turnover rates of catecholamines in the olfactory bulb, hypothalamus, brain stem, hippocampus, striatum, thalamus, cerebral cortex, and spin al cord were determined in rats. Animals were exposed for 2 h to eithe r 60% N2O or air. Immediately following exposure, all animals were inj ected intraperitoneally with alpha-methylparatyrosine (alpha MPT), a c ompetitive inhibitor of tyrosine hydroxylase, and sacrificed at 0, 30, or 90 min postinjection. Brain catecholamine concentrations were dete rmined using high-performance liquid chromatography coupled with elect rochemical detection (HPLCEC). Results indicate that N2O exposure sign ificantly elevates steady-state concentrations of norepinephrine (NE) in the hypothalamus and striatum yet decreases amine levels in the bra in stem region. Steady-state levels of dopamine (DA) were not signific antly altered in any region of the CNS by N2O exposure. Acute exposure to N2O also resulted in significant decreases in the turnover rate of NE in the brain stem, yet it increased turnover of this amine in the olfactory bulb, hypothalamus, and striatum. Acute exposure to N2O resu lted in a decreased turnover rate of DA in the hippocampus and striatu m. In contrast, N2O appears to increase DA turnover in the olfactory b ulb. These results indicate that acute exposure to N2O in rats causes region-specific alterations in steady-state levels and turnover rates of DA and NE within the central nervous system. (C) 1998 Elsevier Scie nce Inc.