Prenatal nicotine exposure increases adrenergic receptor binding in the rat cerebral cortex.
Adult female rats were given nicotine in drinking water for a minimum of 6 weeks prior to mating. The nicotine intake was then maintained at a level of 6.0 +/- 0.2 mg/kg/day throughout pregnancy. At birth the offspring were fostered to control females. Brain noradrenaline levels were elevated in cortex and hypothalamus in infancy but were within the control ranges in adult offspring. However, adrenergic receptor binding was significantly increased in cerebral cortex of adult offspring consistent with the view that prenatal nicotine exposure produces permanent changes in the functioning of central noradrenergic neurons. As in previous studies, the changes were found only in male offspring.
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002540:Cerebral Cortex / Q000378:metabolism*; D003000:Clonidine / Q000494:pharmacology; D004082:Dihydroalprenolol / Q000494:pharmacology; D004146:Dioxanes / Q000494:pharmacology; D005260:Female; D009474:Neurons / Q000378:metabolism; D009538:Nicotine / Q000494:pharmacology*; D009638:Norepinephrine / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000378:metabolism*; D013997:Time Factors
D004146:Dioxanes; D011941:Receptors, Adrenergic; D004082:Dihydroalprenolol; D009538:Nicotine; C010654:(2-(2',6'-dimethoxy)phenoxyethylamino)methylbenzo-1,4-dioxane; D003000:Clonidine; D009638:Norepinephrine