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. 2020 Aug 15;14(1):287–293. doi: 10.1080/19336950.2020.1807851

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© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

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 cited.

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Figure 1. — Long-term potentiation (LTP) is significantly impaired in male CamK2Cre, Ca_v1.2^KO mice without apparent alteration in paired-pulse facilitation or input-output curve. (a) Illustration of the recording scheme. The Schaffer collateral pathway projecting to CA1 neurons was stimulated with bipolar stimulating electrodes. LTP was induced by theta burst stimulation (12TBS; 12 bursts, each of 4 pulses at 100 Hz). (b) Example traces before (blue) and after (red) TBS. LTP (at time 60 min) is substantially reduced in CamK2Cre, Ca_v1.2^KO mice compared to wildtype (WT) littermate controls (166 ± 10% vs. 128 ± 6%, t₍₁₅₎ = 3.549, p = 0.0029). Post-stimulation potentiation (at time 0 min) was also significantly reduced in CamK2Cre, Ca_v1.2^KO mice (180 ± 7% vs. 145 ± 5%, t₍₁₅₎ = 4.220, p = 0.0007). (c)There was no difference in paired pulse facilitation between CamK2Cre, Ca_v1.2^KO mice and WT littermate controls over a wide range of inter-stimulus intervals, indicating intact presynaptic machinery in CamK2Cre, Ca_v1.2^KO mice. (d) Input-output curves with the postsynaptic response (initial slope of field excitatory postsynaptic potential (fEPSP)) plotted as a function of the presynaptic fiber volley amplitude were indistinguishable between CamK2Cre, Ca_v1.2^KO mice and WT mice, indicating intact baseline synaptic transmission.