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. 2016 Aug 4;19(12):pyw068. doi: 10.1093/ijnp/pyw068

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© The Author 2016. Published by Oxford University Press on behalf of CINP.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — AM4113 blocks nicotine-induced increases of ventral tegmental area (VTA) dopamine (DA) neuronal activity. (A) Timeline of the experiment. (B) Typical DA action potential waveform. (C) Microphotograph of coronal section through the VTA showing the deposit of pontamine sky blue done at the end of recordings. (D) Raw traces showing an example of baseline activity. (E) Increase in the activity observed 10 minutes after the injection of nicotine in the vehicle/nicotine group. (F) Blocking effect of AM4113 in the AM4113-/nicotine-treated group. (G) Effects of AM4113 (3mg/kg) on VTA DA neuronal firing rate in the vehicle/nicotine (n=10), AM4113/nicotine (n=10), and AM4113/vehicle (n=9) groups. In (H), burst rate (I) and spikes firing in burst (J) (vs vehicle/saline-treated group, n=10), *P<.05, **P<.01, ***P<.001 from vehicle/saline. Note the significant differences in neuronal activity between the vehicle/nicotine and AM4113/nicotine treatments (#P<.05, ##P<.01, ###P<.001). Bars represent mean ± SEM.