Ozone exposure alters 5-hydroxy-indole-acetic acid contents in dialysates from dorsal raphe and medial preoptic area in freely moving rats. Relationships with simultaneous sleep disturbances

• Published in: Chemico-biological interactions 2003-10, Vol.146 (2), p.147-156
• Main Authors: González-Piña, Rigoberto, Alfaro-Rodrı&#x0301, guez, Alfonso
• Format: Article
• Language: English
• Subjects: 5-Hydroxy-indole-acetic acid; Administration, Inhalation; Animals; Behavior, Animal - drug effects; Hydroxyindoleacetic Acid - metabolism; Locomotion; Male; Microdialysis; Ozone; Ozone - administration & dosage; Ozone - toxicity; Preoptic Area - metabolism; Raphe Nuclei - metabolism; Rats; Rats, Wistar; Sleep; Sleep Initiation and Maintenance Disorders - chemically induced; Sleep, REM - drug effects; Wakefulness - drug effects
• ISSN: 0009-2797; 1872-7786
• DOI: 10.1016/S0009-2797(03)00103-0

Ozone (O3) has been reported to affect sleep patterns and also striatal and mesencephalic contents of 5-hydroxy-indole-acetic acid (5-HIAA) in rats. The aim of this work was to elucidate the effects of O3 exposure in rats upon extracellular 5-HIAA levels in the dorsal raphe (DR) and the hypothalamic medial preoptic area (MPO), two structures involved in sleep–wake homeostasis. Exposure to O3 followed a bell-shaped diurnal pattern, similar to that observed in cities with high air pollution levels. The highest O3 concentration employed was 0.5 ppm. Simultaneous polygraphic records were performed to evaluate the concomitant effects of this exposure model on sleep patterns. Results showed that extracellular 5-HIAA levels increased by 28% in the DR (P=0.0213) while paradoxical sleep (PS) decreased by 56% (P=0.0000) during the light O3 exposure phase. A decrease of 32% in 5-HIAA levels in the MPO (P=0.0450), and of 22% in slow wave sleep (SWS) (P=0.0002) and an increase of 21% in wakefulness (P=0.0430) during the dark post-exposure (Dpost) phase were also observed. We propose that the decrease in PS is the behavioral expression of disruptions of serotonergic DR modulation and, that post-exposure effects observed in the MPO can be explained on the basis of the hypothalamic role in the sleep–wake cycle.