Nicotine regulation of the noradrenergic system
Initial Award Abstract
It has been understood for some time now that mothers who smoke during pregnancy are placing there unborn child at risk for a number of cognitive and behavioral deficits, including attention deficit hyperactivity disorder. Animal models have indicated that nicotine is the primary ingredient in tobacco which can affect the brain. Experiments using these models have found that long-term treatment with nicotine causes a number of alterations at the level of the brain cell (neurons) and the overall morphology of the brain. Among these changes is dysregulation of the noradrenergic system, one of the neurotransmitter systems which allows neurons to communicate with one another and send signals throughout the brain. The cerebellum is one area of the brain which receives input from the noradrenergic system and is the region of focus for our studies. The aim of the proposed experiments is to determine the effects of nicotine on the noradrenergic system in the cerebellum. Is nicotine able to alter development of the cerebellum through the noradrenergic system, and if so, how? Using animal models treated with acute and prenatal/early postnatal chronic nicotine, we will address this question by examining alterations in nicotine-stimulated noradrenaline release in the cerebellum and subsequent disruptions in the migration of neurons during development. The proposed studies will provide a better understanding of the specific mechanisms by which behavioral and cognitive disorders are produced by early exposure to nicotine and will further emphasize the health risks of prenatal nicotine exposure as a consequence of maternal tobacco use. |
|Developmental regulation of nicotinic acetylcholine receptor-mediated [3H]Noradrenaline release from rat cerebelium.
|Periodical: Journal of Neurochemistry
|Authors: O'Leary KT, and Leslie FM