Biochemical changes, early brain growth suppression and impaired detour learning in nicotine-treated chicks

摘要: Abstract Fetal growth suppression associated with chronic maternal intake of cigarette smoke is frequently observed in humans and studies using animal models suggest that utero nicotine exposure an important component this suppression. The developing fetal central nervous system (CNS) sensitive to the inhibitory effect morphological as well functional CNS deficits may result from exposure. presented here show during early embryonic development ultimately inhibits ability 7–11 day old chicks learn a detour task. brain caused by paralleled failure embryo express normal developmental increase ornithine decarboxylase (ODC) activity. This biochemical change be germane mechanism nicotine-induced inhibition and/or behavioral changes because appropriate expression ODC activity essential differentiation CNS. In chick embryo, alters several signaling pathways regulate expression. For example, lowers glucose levels causes significant decreases whole cyclic adenosine 3′,5′-monophosphate (cyclic AMP) AMP binding proteins (protein kinase-A regulatory activity). Also, cultured cells, potent mitogen (insulin) induce activity, but, paradoxically, ovo increased insulin stimulated receptor autophosphorylation membranes.