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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: J Neurochem. 2013 Oct 13;127(6):10.1111/jnc.12442. doi: 10.1111/jnc.12442

Fig. 2.

Fig. 2

Long-term nicotine treatment abolishes the nAChR antagonist-induced decrease on single pulse-stimulated dopamine release. Dopamine release [DA]o was measured in the dorsal portion of the accumbens shell in response to single pulse electrical stimulation. Representative traces of [DA]o in the absence (control) and presence of the α6β2* antagonist α-CtxMII (100 nM), the general nAChR blocker Mec (100 μM), and the β2* nAChR antagonist DHβE (100 nM) are shown for vehicle- and nicotine-treated animals. Scale bar represents 10 nM and 0.5 s. Quantitative analyses show that α-CtxMII, Mec, and DHβE similarly affect single pulse-stimulated release in vehicle-treated animals, indicating that nAChR-modulated [DA]o occurs through α6β2* nAChRs. Single pulse-stimulated release was not further decreased in the presence of any of the nAChR antagonists after nicotine treatment. The values represent the mean ± SEM of 3-13 rats. Significance of difference from control release, ***p < 0.001.