Prenatal ozone exposure abolishes stress activation of Fos and tyrosine hydroxylase in the nucleus tractus solitarius of adult rat

• Published in: Neuroscience letters 2009-03, Vol.452 (1), p.75-78
• Main Authors: Boussouar, A., Araneda, S., Hamelin, C., Soulage, C., Kitahama, K., Dalmaz, Y.
• Format: Article
• Language: English
• Subjects: Air pollution; Analysis of Variance; Animals; Cell Count - methods; Confocal microscope; Female; Immobilization stress; Immunohistochemistry; Male; Oncogene Proteins v-fos - metabolism; Oxidative stress; Ozone; Pregnancy; Pregnant rats; Prenatal Exposure Delayed Effects - chemically induced; Prenatal Exposure Delayed Effects - physiopathology; Rats; Restraint, Physical - methods; Solitary Nucleus - metabolism; Stress, Psychological - enzymology; Stress, Psychological - pathology; Tyrosine 3-Monooxygenase - metabolism
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2009.01.027

Ozone (O 3) is widely distributed in the environment, with high levels of air pollution. However, very few studies have documented the effects on postnatal development of O 3 during pregnancy. The long-term effects of prenatal O 3 exposure in rats (0.5 ppm 12 h/day from embryonic day E5 to E20) were evaluated in the adult nucleus tractus solitarius (NTS) regulating respiratory control. Neuronal response was assessed by Fos protein immunolabeling (Fos-IR), and catecholaminergic neuron involvement by tyrosine hydroxylase (TH) labeling (TH-IR). Adult offspring were analyzed at baseline and following immobilization stress (one hour, plus two hours’ recovery); immunolabeling was observed by confocal microscopy. Prenatal O 3 increased the baseline TH gray level per cell ( p < 0.001). In contrast, the number of Fos-IR cells, Fos-IR/TH-IR colabeled cells and proportion of TH double-labeled with Fos remained unchanged. After stress, the TH gray level ( p < 0.001), number of Fos-IR cells ( p < 0.001) and of colabeled Fos-IR/TH-IR cells ( p < 0.05) and percentage of colabeled Fos-IR/TH-IR neurons against TH-IR cells ( p < 0.05) increased in the control group. In prenatal-O 3 rats, immobilization stress abolished these increases and reduced the TH gray level ( p < 0.05), indicating that prenatal O 3 led to loss of adult NTS reactivity to stress. We conclude that long-lasting sequelae were detected in the offspring beyond the prenatal O 3 exposure. Prenatal O 3 left a print on the NTS, revealed by stress. Disruption of neuronal plasticity to new challenge might be suggested.