INTRODUCTION: Prenatal exposure to nicotine can cause many fetal developmental problems. This study determined the influence of nicotine during pregnancy on the development of cognitive behavior in the offspring. METHODS: Nicotine was administered to pregnant rats through implanted osmotic mini-pumps at 6mg/kg/day and flow rate of 60 μl/day for whole pregnancy from gestational day 4. Fetal and offspring body and brain weight was measured. Learning and memory were tested in adult offspring with Morris water maze; Learning and memory-related receptors were measured. RESULTS: The results showed that exposure to prenatal nicotine (PN) not only caused fetal growth restriction, but also had long-term effects on learning and memory in the offspring. The PN offspring exhibited longer escape latency regardless of sex. The number of passing the platform was significantly less in the PN offspring than that of the control. The expression of messenger RNA (mRNA) and protein of N-methyl-D-aspartic acid receptor (NMDAR) in the hippocampus was significantly increased, whereas alpha7 nicotinic acetylcholine receptor (α7 nAChR) protein was decreased with unchanged α7 nAChR mRNA in the PN offspring. CONCLUSION: The data provided novel information on the PN-affected development in learning and memory in the offspring, suggesting that α7 nAChR and NMDAR1 in the hippocampus might be the targets for actions of PN in association with memory impairment.
INTRODUCTION: Prenatal exposure to nicotine can cause many fetal developmental problems. This study determined the influence of nicotine during pregnancy on the development of cognitive behavior in the offspring. METHODS:Nicotine was administered to pregnant rats through implanted osmotic mini-pumps at 6mg/kg/day and flow rate of 60 μl/day for whole pregnancy from gestational day 4. Fetal and offspring body and brain weight was measured. Learning and memory were tested in adult offspring with Morris water maze; Learning and memory-related receptors were measured. RESULTS: The results showed that exposure to prenatal nicotine (PN) not only caused fetal growth restriction, but also had long-term effects on learning and memory in the offspring. The PN offspring exhibited longer escape latency regardless of sex. The number of passing the platform was significantly less in the PN offspring than that of the control. The expression of messenger RNA (mRNA) and protein of N-methyl-D-aspartic acid receptor (NMDAR) in the hippocampus was significantly increased, whereas alpha7 nicotinic acetylcholine receptor (α7 nAChR) protein was decreased with unchanged α7 nAChR mRNA in the PN offspring. CONCLUSION: The data provided novel information on the PN-affected development in learning and memory in the offspring, suggesting that α7 nAChR and NMDAR1 in the hippocampus might be the targets for actions of PN in association with memory impairment.
Authors: Beryl Y T Chung; Warren Bignell; Derek L Jacklin; Boyer D Winters; Craig D C Bailey Journal: J Neurophysiol Date: 2016-08-03 Impact factor: 2.714
Authors: Filip S Polli; Theis H Ipsen; Maitane Caballero-Puntiverio; Tina Becher Østerbøg; Susana Aznar; Jesper T Andreasen; Kristi A Kohlmeier Journal: Mol Neurobiol Date: 2020-01-08 Impact factor: 5.590
Authors: Linda Chang; Kenichi Oishi; Jon Skranes; Steven Buchthal; Eric Cunningham; Robyn Yamakawa; Sara Hayama; Caroline S Jiang; Daniel Alicata; Antonette Hernandez; Christine Cloak; Tricia Wright; Thomas Ernst Journal: JAMA Psychiatry Date: 2016-12-01 Impact factor: 21.596