Abstract
Maternal smoking is a risk factor associated with nicotine abuse, so the effect of perinatal nicotine exposure was studied on the responsiveness to nicotine across adolescence in the rat. Pregnant Sprague-Dawley rats were implanted with s.c. Alzet osmotic minipumps delivering nicotine (l-nicotine hydrogen tartrate, 2 mg/kg/day free base) or vehicle (0.9% saline) on gestational day 7. There was no effect of nicotine on dam weight gain, food consumption, or water consumption or on the number of live pups or weights at the time of birth. Pups were cross-fostered to obtain the following prenatal/postnatal exposure groups: control/control, nicotine/nicotine, nicotine/control, and control/nicotine. On postnatal days 28, 35, 49, and 63, nicotine-stimulated 86Rb+ efflux was measured in synaptosomes prepared from the frontal cortex, hippocampus, striatum (STR), and thalamus (THL), using a previously developed method. Significant effects of treatment and concentration were detected in all four brain regions, and significant effects of age were observed in the STR and THL. Significant interactions of age and treatment were observed in each of the four brain regions. Nicotine-stimulated 86Rb+ efflux peaked during adolescence in control rats. However, perinatal exposure to nicotine eliminated this peak during adolescence. These results are consistent with recent behavioral and receptor binding results from other laboratories and are the first direct evidence at the cellular level that the nicotinic acetylcholine receptor response varies during adolescence and is affected by perinatal nicotine exposure.
Footnotes
-
This work was supported by the Virginia Youth Tobacco Project. Part of this work was presented previously. Britton AF, Vann RE, and Robinson SE (2005) Perinatal nicotine exposure modifies nicotine-stimulated rubidium efflux across adolescence in the rat, in 67th Annual Scientific Meeting of the College on Problems of Drug Dependence; 2005 Jun 18–25; Orlando, FL. College on Problems of Drug Dependence, Philadelphia, PA; Britton AF, Vann RE, and Robinson SE (2005) Perinatal nicotine exposure modifies nicotinic cholinergic receptor (nAChR) response across development in the rat, in 2005 Annual Meeting of the Society for Neuroscience; 2005 Nov 12–16; Washington, DC. Society for Neuroscience, Washington, DC.
-
Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.
-
doi:10.1124/jpet.106.112730.
-
ABBREVIATIONS: nAChR, nicotinic acetylcholine receptor; PND, postnatal day; CTX, frontal cortex; HIP, hippocampus; STR, striatum; THL, thalamus; GD, gestational day; MI, mortality index; ANOVA, analysis of variance; AUC, area under the curve.
-
↵1 Current affiliation: Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Porter Neuroscience Research Center, Bethesda, Maryland.
- Received August 28, 2006.
- Accepted November 10, 2006.
- The American Society for Pharmacology and Experimental Therapeutics
JPET articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|