The effect of prenatal nicotine on mRNA of central cholinergic markers and hematological parameters in rat fetuses.
A number of studies have demonstrated the influence of nicotine on fetal development. This study determined the expression of choline acetyltransferase (ChAT), vesicular acetylcholine transporter (VAChT), and high-affinity choline transporter (CHT1) in the forebrain and hindbrain following chronic prenatal nicotine exposure in the rat fetus (maternal rats were subcutaneously injected with nicotine at different gestation periods). We also measured the effect of chronic nicotine exposure on fetal blood pO(2), pCO(2), pH, Na(+) and K(+) concentrations, as well as lactic acid levels. Maternal nicotine exposure during pregnancy was associated with a decrease in fetal pO(2) coupled with a significant increase in pCO(2) and lactic acid as well as restricted fetal growth. Additionally, maternal nicotine administration also reduced ChAT, VAChT, and CHT1 mRNA levels in the fetal brain. Nicotine-induced fetal hypoxic responses and reduced cholinergic marker expression in the brain were more severe when nicotine was started in early gestation. Our results provide new information about the effects of repeated exposure to nicotine in utero on the expression of central ChAT, VAChT, and CHT1 in the rat fetus. These results indicate that repeated hypoxic episodes or/and a direct effect of nicotine on the central cholinergic system during pregnancy may contribute to brain developmental problems in fetal origin.
Mao
Caiping
C
Perinatal Biology Center, Soochow University School of Medicine, Suzhou, China.
Yuan
Xin
X
Zhang
Hong
H
Lv
Juanxiu
J
Guan
Junchang
J
Miao
Liyan
L
Chen
Linqi
L
Zhang
Yuying
Y
Zhang
Lubo
L
Xu
Zhice
Z
D000818:Animals; D001784:Blood Gas Analysis; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000196:embryology / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000235:genetics; D004573:Electrolytes / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000187:drug effects / Q000378:metabolism; D047109:Fetal Development / Q000187:drug effects*; D005311:Fetal Hypoxia / Q000139:chemically induced; D005333:Fetus / Q000187:drug effects* / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects*; D002534:Hypoxia, Brain / Q000139:chemically induced / Q000196:embryology; D018811:Maternal Exposure / Q000009:adverse effects; D026901:Membrane Transport Proteins / Q000235:genetics; D009538:Nicotine / Q000008:administration & dosage / Q000633:toxicity*; D011247:Pregnancy; D016548:Prosencephalon / Q000187:drug effects / Q000196:embryology / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012249:Rhombencephalon / Q000187:drug effects / Q000196:embryology / Q000378:metabolism; D050494:Vesicular Acetylcholine Transport Proteins / Q000235:genetics
D004573:Electrolytes; D026901:Membrane Transport Proteins; D012333:RNA, Messenger; D050494:Vesicular Acetylcholine Transport Proteins; C065637:choline transporter; D009538:Nicotine; D002795:Choline O-Acetyltransferase