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. 2014 Nov 11;2:147. doi: 10.1186/s40478-014-0147-1

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© Molas et al.; licensee BioMed Central Ltd. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Electrically induced synaptic plasticity of Shaffer collateral-CA1 pathway. (a) High frequency stimulation (HFS; 100Hz, 1s) induced synaptic potentiation at Schaffer Collateral (SC)-CA1 synapses similarly in slices from saline (Sal)-treated wild type (WT) and TgCHRNA5/A3/B4 (Tg) mice. Chronic nicotine (Nic, 3.25 mg/Kg/d) administration for 7 d enhanced synaptic potentiation both in WT and Tg mice. Upper panel: representative field excitatory postsynaptic potentials (fEPSPs) in response to one stimulation in the CA1 stratum radiatum before (1) and 15 min after (2) applying HFS (arrow), Scale bar 0.5 mV and 1 ms. Lower panel: slopes of the fEPSPs normalized to those obtained before applying HFS (%). (b) Mean values of fEPSPs potentiation at 15 and 45 min after HFS. (c) The paired pulse ratio (fEPSP2/fEPSP1) with an inter-pulse interval of 50 ms (response average of 5 paired pulses; time interval 1 s) was similar among slices from the different experimental conditions (n = 3–5 recordings/animal; 4 – 5 animals/group from ≥ 3 experiments). Two-way ANOVA treatment effect ωω p ≤ 0.01.