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. 2016 Feb 2;3(1):ENEURO.0095-15.2015. doi: 10.1523/ENEURO.0095-15.2015

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Copyright © 2016 Storey et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 7. — Nicotine in vitro blocks CPD through α7*- and α4β2*-type nicotinic receptors. A, Responses of individual MSNs show that nicotine inhibited corticostriatal activity in saline-treated mice by (B) reducing high-frequency, low-amplitude mEPSCs, but had no effect on their amplitude distribution (inset). For B, E, J, *p<0.05, Bonferroni t test; for all other panels, *p<0.05, paired t test and ^$$p<0.01, Student’s t test. C, The frequency distribution (left) and the average peak frequency (right) of mEPSCs. Nicotine increased low-frequency mEPSCs in saline-treated mice. D, Nicotine increased the frequency of mEPSCs in MSNs from amphetamine self-administering mice by (E) augmenting high-frequency, low-amplitude mEPSCs, while having no effect on their amplitude distribution (inset). F, The frequency distribution (left) and average peak frequency (right) of mEPSCs. Nicotine reduced low-frequency mEPSCs in amphetamine self-administering mice. G, Mean±SE frequencies of mEPSCs from saline-treated and amphetamine self-administering mice in response to nicotine. H, The frequency distribution (left) and average peak frequencies (right) compares mEPSCs in MSNs from saline-treated mice with those from amphetamine self-administering mice exposed to nicotine in vitro. I, The α4β2*-type receptor antagonist DHβE blocked the synaptic depression generated by nicotine and (J) increased high-frequency, low-amplitude synaptic events. K, The α7*-type nicotinic receptor antagonist MLA reduced (L) high-frequency, low-amplitude mEPSCs. J, L, Insets show similar mEPSC amplitude distributions.