| Literature DB >> 24968237 |
Li Wang1, Shujiang Shang1, Xinjiang Kang1, Sasa Teng2, Feipeng Zhu2, Bin Liu2, Qihui Wu2, Mingli Li2, Wei Liu2, Huadong Xu2, Li Zhou2, Ruiying Jiao2, Haiqiang Dou2, Panli Zuo2, Xiaoyu Zhang2, Lianghong Zheng2, Shirong Wang2, Changhe Wang2, Zhuan Zhou2.
Abstract
Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevant levels of nicotine modulate striatal DA release. The optogenetic stimulation of ChIs elicits DA release, which is potently inhibited by nicotine with an IC50 of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by α6β2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP(DA)-dependent DA release (AP(DA), AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine's effects on striatal DA release.Entities:
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Year: 2014 PMID： 24968237 DOI： 10.1038/ncomms4925
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919