Disruption of neostriatal development in rats following perinatal exposure to mild, but chronic carbon monoxide.
The vulnerability of the developing neostriatum to mild, but chronic hypoxia was evaluated in weanling rats exposed only in utero or from conception through postnatal day 10 to 0, 75, 150, and 300 ppm carbon monoxide (CO). The exposure conditions produced maternal carboxyhemoglobin (HbCO) levels of about 11, 19, and 27 percent. HbCO levels of 5 percent are maintained by human cigarette smokers while comparable levels in non-smokers average less than 1%. Significant elevations in DNA and the neurotransmitter, dopamine (DA), were observed in the striatum of 21-day-old rats following the combined pre- and neonatal CO exposure. These neurochemical changes were observed 11 days after CO exposure was terminated and, therefore, cannot be interpreted as acute responses to reduced oxygen. These data indicate that the immature neostriatum is altered by even mild hypoxic insults presented during the time of neuronal proliferation and synaptogenesis.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects; D002249:Carbon Monoxide Poisoning / Q000503:physiopathology*; D002421:Caudate Nucleus / Q000254:growth & development*; D004298:Dopamine / Q000378:metabolism; D006719:Homovanillic Acid / Q000378:metabolism; D008297:Male; D018377:Neurotransmitter Agents / Q000378:metabolism; D011699:Putamen / Q000254:growth & development*; D051381:Rats
D018377:Neurotransmitter Agents; D015102:3,4-Dihydroxyphenylacetic Acid; D004298:Dopamine; D006719:Homovanillic Acid