Functional sequelae of developmental exposure to mild concentration of carbon monoxide in rats

The results of our recent studies dealing with the effects on the central (CNS) and peripheral (PNS) nervous system induced in rat offspring by prenatal exposure to relatively mild CO concentrations (75 and 150 ppm) have been reviewed in the present paper. Gestational exposure to CO has been shown to produce the following behavioral changes: (I) altered ontogeny of emotional reactivity, as shown by the reduction in the minimum frequency of ultrasonic calls emitted by rat pups removed from their nest and by the decrease in ultrasonic responsiveness to a challenge dose of diazepam; (2) irreversible alterations in cognitive function. Prenatal CO exposure also impairs PNS development. In particular, inactivation of sodium channels responsible for generation and propagation of action potentials is slowed down and reversal potential of sodium current is shifted towards negative values. More recent data have shown that the sensitivity of Na channels to the blocking activity of tetrodotoxin is also affected. Moreover, gestational CO exposure alters peripheral myelinogenesis. In particular, the rate of myelin formation and myelin basic protein expression are severely impaired. These results point out the extraordinary vulnerability of the fetus to CO and the large risk to which the smoking mother exposes her offspring.