title: Neonatal nicotine exposure alters hippocampal EEG and event-related potentials (ERPs) in rats.
abstract: A consensus is forming that nicotine can damage the developing rat central nervous system. However, few studies have assessed the electrophysiological effects of neonatal nicotine exposure in rodents in brain regions known to be sensitive to the teratogenic properties of nicotine. In a previous study it was reported that 1.0 and 4.0 mg/kg/day nicotine exposure from postnatal days 4-9, a developmental period corresponding to human third-trimester exposure, significantly altered hippocampal event-related potentials (ERPs) but did not effect cortical ERPs, cortical EEG, or hippocampal EEG. Because alterations in behavior and cortical/hippocampal neurochemistry and morphology have been reported following nicotine exposure, the present study used a higher dose of nicotine during the postnatal period (6.0 mg/kg/day) determine if functional changes in the EEG of these regions might contribute to behavioral changes that have been observed. Male Sprague-Dawley rats were exposed to 6. 0 mg/kg/day nicotine via gastric infusion using an artificial rearing, "pup-in-the-cup," technique for 6 consecutive days (postnatal days 4-9). At adulthood, EEG and auditory ERPs were recorded from the cortex and hippocampus. There were no significant differences in EEG or ERPs recorded from the cortex between nicotine-treated and control subjects. Examination of the hippocampal EEG revealed significantly decreased power in the 1-2-Hz frequency band of nicotine-treated rats. In addition, there was a significantly attenuated P300 ERP response to a noise tone in the nicotine-treated rats compared to controls. These data indicate that neonatal nicotine exposure alters functional activity in the hippocampus of adult rats. These effects are likely to be the result of synaptic disorganization in the hippocampus, and indicate that neonatal nicotine exposure exerts teratogenic effects on the developing central nervous system, particularly the hippocampus, which persist into adulthood.
authors.affiliation: The Scripps Research Institute, Department of Neuropharmacology, La Jolla, CA 902037, USA.
authors.forename: C J
authors.initials: CJ
authors.lastname: Slawecki
authors.forename: J D
authors.initials: JD
authors.lastname: Thomas
authors.forename: E P
authors.initials: EP
authors.lastname: Riley
authors.forename: C L
authors.initials: CL
authors.lastname: Ehlers
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology; D004569:Electroencephalography / Q000187:drug effects*; D004594:Electrophysiology; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013238:Stereotaxic Techniques
chemical_list: D018722:Nicotinic Agonists; D009538:Nicotine