Growth Impairment of the Fetal Nervous System by Nicotinic Stimulation
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The maternal utilization of tobacco substances during pregnancy gives rise to growth retardation and an array of neurobehavior defects in the offspring. Although concurrent exposure of the fetus to hypoxia and ischemia are major contributors to the developmental effects of smoking in man, or of injected nicotine in animals, recent studies using slow infusions of nicotine strongly suggest that nicotine affects fetal and neonatal development. Due to the action of nicotine via neurotransmitter receptors in the nervous system) the sensitivity of the developing brain is displayed in the disruption of cellular development and blunting of neural activity in central and peripheral catecholaminergic systems (Navarro et al, p894).
Many of the developmental abnormalities seen with prenatal nicotine exposure resemble those obtained through enhancement of cholinergic neuronal activity through dietary manipulations. Endogenous cholinergic input has been shown to control cellular development in cerebral cortex, the same region found to be highly sensitive to perturbations caused by nicotine or by high dietary choline. Thus, the effects of nicotine may represent the simulation of a natural developmental signal, but at an inappropriate time. A current study examines the potential interaction of prenatal nicotine exposure with the development of cholinergic neurotransmitter systems in different brain regions (Navarro et al’ p894).
The experimentation of the pregnant Sprague-Dawley rats entailed a nicotine infusion pump being placed on the control and experimental pregnant rats. Initially the nicotine infusion inhibited maternal weight gain for the first few days of implantation. Normal weight gains ensued thereafter. The nicotine had no significant effect on the proportion of pups delivered (82% in controls’ 83% in the nicotine group). At 16 days of gestation, little or no alterations of body or brain weight can be attributed to the nicotine infusion. Postnatally, there were small (5-10%) but statistically significant lags in body and brain region weights in the nicotine group, all the weight differences were resolved by the 2nd postnatal week. The ChAT activity showed distinct regional differences in development. In the cerebral cortex, the rise in activity occurred most rapidly during the 2nd to 3rd postnatal weeks; levels achieved half of the adult value by the middle to end of the 3rd week and reached adult levels at about 6 weeks postpartum. Midbrain and brainstem displayed a slightly earlier developmental profile, reaching half of adult values by the end of the 2nd week or middle of the 3rd week. The pattern in the cerebellum was different from the others,...