Prenatal adverse effects of nicotine on the developing brain

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

“…It should be noted that the pump, marketed as a 2-week infusion device, actually takes 17.5 days to be exhausted completely (information supplied by the manufacturer) and thus the nicotine infusion terminates during GD21. Maternal plasma nicotine levels achieved with this administration model resemble those seen in heavy smokers (25-60 ng/ml) as characterized previously (Isaac and Rand, 1972;Levin and Slotkin, 1998;Lichtensteiger et al, 1988;Murrin et al, 1985;Slotkin, 1992Slotkin, , 1998Slotkin, , 1999Slotkin, , 2004). This animal model also resembles the effects of maternal smoking in that fetal nicotine levels exceed those found in maternal plasma (Luck et al, 1985;Sarasin et al, 2003).…”

“…The nicotine exposure period thus spans the recognized boundaries of adolescence in the rat, as typified by endocrine, pubertal, and behavioral parameters (Spear, 2000). In the adolescent rat this paradigm produces plasma nicotine levels of 25 ng/ ml, similar to that in typical smokers (Lichtensteiger et al, 1988;Trauth et al, 2000b); it produces a transient (10%) reduction in body weight during treatment, an effect that disappears after termination of the infusion (Abreu-Villaça et al, 2003a;Trauth et al, 1999). Studies were conducted at four time points, one during adolescent nicotine administration (PN45) and three during the withdrawal period (PN50, PN60, and PN75).…”

Short-Term Adolescent Nicotine Exposure has Immediate and Persistent Effects on Cholinergic Systems: Critical Periods, Patterns of Exposure, Dose Thresholds

“…At the highest dose rate, this paradigm produces plasma nicotine levels similar to those in typical smokers, approximately 25 ng/ml (Trauth et al, 2000b). All the treatments were within the range over which the plasma nicotine level is linear with the dose rate (Lichtensteiger et al, 1988), so that at the intermediate and lower doses, concentrations were about 8 and 2.5 ng/ml, respectively. The lowest concentration is thus ten times below that found in regular smokers, and well within the range of those with exposure to ETS (Eliopoulos et al, 1996;Fried et al, 1995;Jauniaux et al, 1999;Kohler et al, 1999;Ostrea et al, 1994).…”

“…To evaluate the role of different patterns of nicotine exposure (continuous vs intermittent), we contrasted two different routes of administration: infusions via implanted osmotic minipumps and twice-daily subcutaneous injections. Nicotine was administered at three different doses (0.6, 2, and 6 mg/ kg/day) that, with the infusion model, elicit plasma levels ranging from as little as 2.5-25 ng/ml (Lichtensteiger et al, 1988;Trauth et al, 2000b). In light of the unique behavioral sensitization seen in early adolescence , we concentrated on exposure beginning on postnatal day (PN) 30, which, on the basis of brain development, onset of puberty, and patterns of drug reactivity, represents the early adolescent stage in the rat (Spear, 2000).…”

Prenatal Exposure to Maternal Cigarette Smoking and the Adolescent Cerebral Cortex

“…Kallen (2000) analyzed the Swedish Medical Birth Registry (1983)(1984)(1985)(1986)(1987)(1988)(1989)(1990)(1991)(1992)(1993)(1994)(1995)(1996): 1 362 169 infants) and found significant negative correlation between PEMCS and head circumference at birth. Neuroanatomical studies carried out in experimental animals exposed prenatally to nicotine showed nicotine-induced acute and chronic changes in cholinergic, catecholaminergic, and other neurotransmitter systems (Lichtensteiger et al, 1988;Slotkin, 1998Slotkin, , 2004. In terms of brain structure, Sabherwal (1994, 1998) observed a significant reduction in brain weight, cortical thickness in the somatosensory cortex, neural density in layer V of the somatosensory cortex, and the neural area of the dentate gyrus, CA1, and CA3 regions of the hippocampus.…”