期刊
CELL
卷 127, 期 3, 页码 621-633出版社
CELL PRESS
DOI: 10.1016/j.cell.2006.09.035
关键词
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资金
- NEI NIH HHS [T32 EY017878, T32EY017878] Funding Source: Medline
- NIDA NIH HHS [R01 DA018341, 7R01DA018341-02] Funding Source: Medline
- NIGMS NIH HHS [R01 GM078276, T32GM008322, T32 GM008322, R01 GM078276-01] Funding Source: Medline
Nicotine, the primary addictive substance in tobacco, induces profound behavioral responses in mammals, but the underlying genetic mechanisms are riot well understood. Here we develop a C. elegans model of nicotine-dependent behavior. We show that worms exhibit behavioral responses to nicotine that parallel those observed in mammals, including acute response, tolerance, withdrawal, and sensitization. These Nicotine responses require nicotinic acetylcholine receptor (nAChR) family genes that are known to mediate nicotine dependence in mammals, suggesting functional conservation of nAChRs in nicotine responses. Importantly, we find that mutant worms lacking TRPC (transient receptor potential canonical) channels are defective in their response to nicotine and that such a defect can be rescued by a human TRPC channel, revealing an unexpected role or TRPC channels in regulating nicotine-dependent behavior. Thus, C. elegans can be used to characterize known genes as well as to identify new genes regulating nicotine responses.
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