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. 2020 Aug 11;12:230. doi: 10.3389/fnagi.2020.00230

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Copyright © 2020 Calabrese, Di Maio, Marino, Cardinale, Natale, De Rosa, Campanelli, Mancini, Napolitano, Avallone, Calabresi, Usiello, Ghiglieri and Picconi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Synaptic plasticity in spiny projection neurons (SPNs) of L-DOPA vs. rapamycin + L-DOPA-treated rats. (A, left panel) Current-voltage curves obtained during current-clamp recordings of SPNs for each experimental group. (A, right panel) Tonic firings of SPNs obtained through intracellular and whole-cell patch clamp recordings of corticostriatal slices from animals treated with L-DOPA (green line) and with a combination of rapamycin plus L-DOPA (red line), in response to hyperpolarizing and depolarizing current pulses. (B, left panel) Time course of the high-frequency stimulation (HFS)-induced long-term potentiation (LTP) and low-frequency stimulation (LFS)-induced depotentiation in corticostriatal SPNs. (B, right panel) Representative corticostriatal excitatory postsynaptic potential (EPSP) amplitude traces showing the recovery of the LTP in each experimental group (L-DOPA and rapamycin + L-DOPA). The application of a HFS protocol induced LTP in both groups (L-DOPA ##p < 0.01; rapamycin + L-DOPA ***p < 0.001). LFS induced depotentiation only in the group treated with both rapamycin and L-DOPA (*p < 0.05 compared to 8-10 min post HFS; **p < 0.01 compared to L-DOPA alone group).