Developmental nicotine exposure impairs memory and reduces acetylcholine levels in the hippocampus of mice

Abstract

Nicotine is a strong psychoactive and addictive compound found in tobacco. Use of nicotine in the form of smoking, vaping or other less common methods during pregnancy has been shown to be related to poor health conditions, including cognitive problems, in babies and children. However, mechanisms of such cognitive deficits are not fully understood. In this study we analyzed hippocampus dependent cognitive deficits using a mouse model of developmental nicotine exposure. Pregnant dams were exposed to nicotine and experiments were performed in one month old offspring. Our results show that nicotine exposure did not affect locomotor behavior in mice. Hippocampus dependent working memory and object location memory were diminished in nicotine exposed mice. Furthermore, acetylcholine levels in the hippocampus of nicotine exposed mice were reduced along with reduced activity of acetylcholinesterase enzyme. Analysis of transcripts for proteins that are known to regulate acetylcholine levels revealed a decline in mRNA levels of high affinity choline transporters in the hippocampus of nicotine exposed mice but those of vesicular acetylcholine transporter, choline acetyltransferase, and α7-nicotinic acetylcholine receptors were not altered. These results suggest that developmental nicotine exposure impairs hippocampus dependent memory forms and this effect is likely mediated by altered cholinergic function.