Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-0

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>f EPSPs, followed by recovery and stabilization (n = 15). (B) NR2B inhibitors, Ro25-6981 (0.5 μM) or Ifenprodil (3 μM), do not affect NMDA-induced plasticity (n = 8+4 = 12). (C) In presence of NR2A inhibitor, NVP-AAM077 (0.4 μM), NMDA effects are different compared with control situation, with a shorter recovery phase and much less depression (n = 10). (D) Bar diagram reveals LTD at 60 min after NMDA application as percentage of the initial baseline under the different experimental conditions in A-C. Data are given as mean ± S.E.M. Black bars in A-C indicate the duration of drug treatment. Values are shown averaged for 2 min periods. Inserts illustrate EPSP-traces taken at the indicated time points (a, b). Calibrations: 0.5 mV, 10 ms

Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-1

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>g baseline responses, defining the 100% level (1), applying NR2A inhibitor NVP-AAM077 (0.4 μM) leads to a substantial reduction of the isolated NMDA response (2). Adding NR2B inhibitor Ro25-6981 (0.5 μM) further depresses the responses down to near zero (3). Subsequent perfusion with AP5 (50 μM) fully blocks the synaptic responses and values obtained in this solution are taken as zero level (4). (ii) Traces 1–3 plotted together after subtraction of the zero level. (iii) Bar diagram quantifying the reductions of NMDA-EPSPs after sequentially adding the two subunit-specific blockers, NVP-AAM077 and Ro25-6981. (B) Similar plots for another set of experiments where the two blockers were applied in a different order (n = 6). The bar diagrams show data as mean ± S.E.M. Calibrations: 0.1 mV, 20 ms

Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-7

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>f EPSPs, followed by recovery and stabilization (n = 15). (B) NR2B inhibitors, Ro25-6981 (0.5 μM) or Ifenprodil (3 μM), do not affect NMDA-induced plasticity (n = 8+4 = 12). (C) In presence of NR2A inhibitor, NVP-AAM077 (0.4 μM), NMDA effects are different compared with control situation, with a shorter recovery phase and much less depression (n = 10). (D) Bar diagram reveals LTD at 60 min after NMDA application as percentage of the initial baseline under the different experimental conditions in A-C. Data are given as mean ± S.E.M. Black bars in A-C indicate the duration of drug treatment. Values are shown averaged for 2 min periods. Inserts illustrate EPSP-traces taken at the indicated time points (a, b). Calibrations: 0.5 mV, 10 ms

Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-6

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>ing Mgconcentration (0.1 instead of 1.3 mM; n = 6). (B) Bar diagram shows NMDA-induced LTD in different Mgsolutions. Dashed bar is control data from Fig. 1D. (C) In a "slow LTD" experiment, similar to that in Fig. 3C, lowering the concentration of Mgin the perfusion solution (0.01 instead of 0.1 mM) helps with the induction of "slow LTD" in presence of NVP-AAM077 (0.4 μM; n = 7). (D) Bar diagram reveals the "slow LTD" induced in different Mgsolutions. Dashed bar is control data from Fig. 3D. (E) Similarly, using low Mgsolution (0.1 instead of 1.3 mM) in LTP experiments (compare Fig. 4C) enables a small potentiation of EPSPs under inhibition of NR2A subunits by NVP-AAM077 (n = 7). (F) Bar diagram shows LTP induced in different Mgsolutions. Dashed bar is control data from Fig. 4D. Data are shown as mean ± SEM. Inserts show the EPSP-traces taken at the indicated time points (a-d). Calibrations: 0.5 mV (A, E), 0.2 mV (C), 20 ms

Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-2

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>on. The experiment consists of preinduction baseline level in presence of a high concentration of AP5 (50 μM), induction period in AP5-free solution, and established LTD after reintroduction of high AP5. AMPA component (black symbols) and NMDA component (gray symbols) are plotted as functions of time, each point indicating the average in 2 min (n = 8 experiments). (B) A similar result is obtained in the same type of experiment but treated with Ro25-6981 (0.5 μM; n = 8) during the induction period. (C) The "slow LTD" is substantially blocked when NVP-AAM077 (0.4 μM; n = 7) is present under induction in AP5-free solution. (D) Bar diagram shows the "slow LTD" at 30 min after reintroducing AP5, plotted as percentage of the preinduction level under the three different experimental situations in A-C. Data are mean ± S.E.M. Black bars in A-C indicate the duration of drug treatment. Inserts show the EPSP-traces taken at the indicated time points (a-d) and the timing of the measurements for AMPA and NMDA components (0–1.5 ms after fiber volley and at 35–45 ms, respectively; see bars below traces). Calibrations: 0.2 mV, 20 ms

Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-3

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>n. The EPSP is potentiated to a near doubling of the initial response. Test pathway (black symbols) and control pathway (gray symbols) are plotted as functions of time, each point indicating the average in 1 min (n = 10 experiments). (B) LTP is partially blocked by Ro25-6981 (0.5 μM; n = 2)/Ifenprodil (3 μM; n = 4) (total n = 6). (C) LTP is fully prevented when NVP-AAM077 (0.4 μM) is present (n = 5). (D) Bar diagram summarizes the data in A-C with mean ± S.E.M. LTP is measured at 60 min after tetanization relative to the initial baseline. Arrows in A-C indicate the tetani. Black bars indicate the duration of drug application. Inserts illustrate EPSP-traces taken at the indicated time points (a, b). Calibrations: 0.5 mV, 20 ms

Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity-4

<p><b>Copyright information:</b></p><p>Taken from "Role of NMDA receptor subtypes in different forms of NMDA-dependent synaptic plasticity"</p><p>http://www.biomedcentral.com/1471-2202/8/55</p><p>BMC Neuroscience 2007;8():55-55.</p><p>Published online 26 Jul 2007</p><p>PMCID:PMC1959237.</p><p></p>ear doubling of the EPSP. Subsequent application of NMDA (30 μM, 4 min) leads to persistent depression of the control pathway (gray symbols) and depotentiation of the test pathway (black symbols). Secondary tetanization of the test pathway causes a repotentiation, lifting the test responses back to a potentiated level (n = 12). (B) and (C) show similar experiments but treated with Ro25-6981 (0.5 μM; n = 4)/Ifenprodil (3 μM; n = 2) (total n = 6) or NVP-AAM077 (0.4 μM; n = 5) shortly after LTP induction. Both depotentiation and repotentiation are preferentially attenuated by NVP-AAM077 as compared to Ro25-6981/Ifenprodil. Arrows indicate the tetani. Black bars indicate the duration of drug application