Maternal nicotine exposure: Effect on physical development and fine motor coordination of the rat offspring

Estelle Lacoste Robinson


The purpose of the present study was to measure the effect of chronic maternal nicotine consumption during gestation only, gestation continuing through lactation, lactation only, and a no-drug control group on physical development, and gross and fine motor coordination of the offspring. To more precisely measure the dose response curve, three dose levels of nicotine (3.0, 2.25, 1.5mg/kg) were administered along with a saline control group. Nicotine was administered via an osmotic minipump. Gravid rats were randomly assigned to one of the four conditions. The pump was implanted on postnatal day 14. The offspring studied were male Sprague-Dawley rats 1 to 22 days old. Half of the pups from each litter were cross fostered to isolate the drug effect prenatally. Maturational parameters were pinna detachment, incisor eruption, and eye opening. Gross motor coordination measures were surface righting, negative geotaxis, swimming ontogeny, and open field. Measures of fine motor coordination were roto rod and beam walking. It was hypothesized that time of maternal drug exposure and dose level would affect physical development and gross and fine motor coordination differentially. Delayed swimming development provided evidence for a teratogenic effect of maternal nicotine consumption. No significant differences were observed in physical development or gross motor coordination. The beam walk, roto rod, swimming ontogeny, and open field provided significant evidence that maternal nicotine consumption delays fine motor coordination. Results showed that the most damaging effects of maternal nicotine consumption occur during gestation. The strongest effect occurred at 3.0mg/kg during gestation/lactation, with the second strongest effect occurring at 3.0mg/kg during gestation. Nicotine exposure during lactation potentiates the damage which occurred during gestation. A behavioral effect from nicotine exposure during lactation occurred at 1.5 and 2.25mg/kg. Development was facilitated at 1.5mg/kg, inhibited at 3.0mg/kg, while a dose of 2.25mg/kg oscillated between facilitating or inhibiting. The results of the present study, therefore, suggest that a dose level of 2.25mg/kg is near the apex of the dose-response curve.