These authors contributed equally to this work.
Nicotine-motivated behavior in Caenorhabditis elegans requires the nicotinic acetylcholine receptor subunits acr-5 and acr-15
Article first published online: 25 JAN 2013
© 2013 Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 37, Issue 5, pages 743–756, March 2013
How to Cite
Sellings, L., Pereira, S., Qian, C., Dixon-McDougall, T., Nowak, C., Zhao, B., Tyndale, R. F. and van der Kooy, D. (2013), Nicotine-motivated behavior in Caenorhabditis elegans requires the nicotinic acetylcholine receptor subunits acr-5 and acr-15. European Journal of Neuroscience, 37: 743–756. doi: 10.1111/ejn.12099
- Issue published online: 4 MAR 2013
- Article first published online: 25 JAN 2013
- Manuscript Accepted: 19 NOV 2012
- Manuscript Revised: 19 OCT 2012
- Manuscript Received: 11 JUL 2011
- invertebrate animal model;
- nicotinic acetylcholine receptor;
Signaling at nicotinic acetylcholine receptors in Caenorhabditis elegans controls many behaviors, including egg-laying and locomotor activity. Here, we show that C. elegans approaches a point source of nicotine in a time-, concentration- and age-dependent manner. Additionally, nicotine paired with butanone under starvation conditions prevented the reduced approach to butanone that is observed when butanone is paired with starvation alone and pairing with nicotine generates a preference for the tastes of either sodium or chloride over baseline. These results suggest nicotine acts as a rewarding substance in C. elegans. Furthermore, the nicotinic receptor antagonist mecamylamine, the smoking cessation pharmacotherapy varenicline, mutation of the dop-1 and dop-2 dopamine receptors, and mutations of either acr-5 or acr-15, two nicotinic receptor subunit genes with sequence homology to the mammalian α7 subunit, all reduced the nicotine approach behavior. These two mutants also were defective at associating the presence of nicotine with butanone under starvation conditions and acr-5 mutation could obviate the effect of pairing nicotine with salts. Furthermore, the approach deficit in acr-15 mutants was rescued by selective re-expression in a subset of neurons, but not in muscle. Caenorhabditis elegans may therefore serve as a useful model organism for nicotine-motivated behaviors that could aid in the identification of novel nicotine motivational molecular pathways and consequently the development of novel cessation aids.