glun2d ko mice Search Results


glun2d ko mice  (Charles River Laboratories)
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Charles River Laboratories glun2d ko mice
Comparison of baseline synaptic transmission and PPF of WTs and <t>GluN2D</t> KOs. (A) FV amplitude plotted against stimulus intensity. Slopes of WT line (−0.048 mV/stim intensity, n = 14) and KO line (−0.051 mV/stim intensity, n = 13) were not significantly different (F(1, 239) = 0.5774, p = 0.448, F test). (B) fEPSP to FV relationship for WT (slope of line = 1.8 ms −1 , n = 15) and KO (slope of line = 1.9 ms −1 , n = 11) were not significantly different (F(1, 15) = 0.9132, p = 0.3544, F test). (C) PPF (50 ms inter-pulse interval) was not significantly different between WTs (2.1 ± 0.07, n = 15) and KOs (2.1 ± 0.06, n = 15, t(28) = 0.2460, p = 0.8075, t -test). (D) Representative fEPSP traces from points indicated in A. (E) Representative fEPSP traces showing PPF in WTs (black) and GluN2D KOs (grey).
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Comparison of baseline synaptic transmission and PPF of WTs and GluN2D KOs. (A) FV amplitude plotted against stimulus intensity. Slopes of WT line (−0.048 mV/stim intensity, n = 14) and KO line (−0.051 mV/stim intensity, n = 13) were not significantly different (F(1, 239) = 0.5774, p = 0.448, F test). (B) fEPSP to FV relationship for WT (slope of line = 1.8 ms −1 , n = 15) and KO (slope of line = 1.9 ms −1 , n = 11) were not significantly different (F(1, 15) = 0.9132, p = 0.3544, F test). (C) PPF (50 ms inter-pulse interval) was not significantly different between WTs (2.1 ± 0.07, n = 15) and KOs (2.1 ± 0.06, n = 15, t(28) = 0.2460, p = 0.8075, t -test). (D) Representative fEPSP traces from points indicated in A. (E) Representative fEPSP traces showing PPF in WTs (black) and GluN2D KOs (grey).

Journal: Neuropharmacology

Article Title: Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

doi: 10.1016/j.neuropharm.2021.108833

Figure Lengend Snippet: Comparison of baseline synaptic transmission and PPF of WTs and GluN2D KOs. (A) FV amplitude plotted against stimulus intensity. Slopes of WT line (−0.048 mV/stim intensity, n = 14) and KO line (−0.051 mV/stim intensity, n = 13) were not significantly different (F(1, 239) = 0.5774, p = 0.448, F test). (B) fEPSP to FV relationship for WT (slope of line = 1.8 ms −1 , n = 15) and KO (slope of line = 1.9 ms −1 , n = 11) were not significantly different (F(1, 15) = 0.9132, p = 0.3544, F test). (C) PPF (50 ms inter-pulse interval) was not significantly different between WTs (2.1 ± 0.07, n = 15) and KOs (2.1 ± 0.06, n = 15, t(28) = 0.2460, p = 0.8075, t -test). (D) Representative fEPSP traces from points indicated in A. (E) Representative fEPSP traces showing PPF in WTs (black) and GluN2D KOs (grey).

Article Snippet: The global GluN2D KO mice were obtained from Professor Masayoshi Mishina (University of Kyoto) and maintained at a breeding facility in the UK (Charles River).

Techniques: Comparison, Transmission Assay

Altered synaptic plasticity in GluN2D KOs. (A) Pooled data showing the time course of potentiation of fEPSPs (mean ± SEM) for WTs (filled circles, n = 21) and KOs (open circles, n = 17). Decay of STP was fitted using a bi-exponential decay function (black curve fits WT and grey curve fits KO). The rate of decay of STP1 and STP2 were not significantly different between WTs (τ 1 = 3.0 min, τ2 = 24.0 min) and KOs (τ 1 = 4.7 min, τ2 = 25.8 min) (τ 1 F(1, 3333) = 1.231, p = 0.267, τ 2 F(1, 3333) = 0.0801, p = 0.777, F test). In this and subsequent time course plots, the arrowhead indicates the time of high frequency stimulation and the associated “B” refers to the number of bursts delivered. Representative fEPSPs from WTs and KOs at the time-points indicated in A are shown on the right. (B) The level of STP1 and STP2 were calculated by integrating the fast and slow components of the bi-exponential decay function, respectively, and are presented normalised with respect to the corresponding control. STP1 was significantly lower in WTs (100.0 ± 10.1%) compared to KOs (212.4 ± 19.4%; ****p < 0.0001, t(36) = 5.431, t -test). STP2 was not significantly different between WTs (100.0 ± 13.0%) and KOs (138.7 ± 15.7%; p = 0.0633, t(36) = 1.916, t -test). LTP in WTs (38.5 ± 4.3%) was significantly less than in KOs (52.5 ± 5.5%; t(36) = 2.055, *p = 0.0472, t -test) (C) Time course of potentiation in WTs (filled circles, n = 4) and KOs (open circles, n = 5) in the presence of GABA A and GABA B receptor antagonists. Decay time constant of STP1 and STP2 were not different between WTs (τ 1 = 1.7 min, τ 2 = 19.2 min) and KOs (τ 1 = 2.1 min, τ 2 = 25.1 min; τ 1 F(1, 796) = 1.081, p = 0.299; τ 2 F(1, 796) = 1.172, p = 0.279, F test). In this and subsequent figures, horizontal bars on the time course plots indicates the duration of compound application. (D) STP1 level was significantly lower in WT (100 ± 8.8%) compared to KOs (191.6 ± 32.2%; *p = 0.0437, t(7) = 2.456, t -test). STP2 was significantly greater in WTs (100 ± 13.4%) compared to KOs (45.5 ± 14.5%; *p = 0.0309, t(7) = 2.694, t -test). LTP was similar in WTs (79.4 ± 8.1%) and KOs (67.4 ± 10.7%; t(7) = 0.8548, p = 0.421; t -test).

Journal: Neuropharmacology

Article Title: Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

doi: 10.1016/j.neuropharm.2021.108833

Figure Lengend Snippet: Altered synaptic plasticity in GluN2D KOs. (A) Pooled data showing the time course of potentiation of fEPSPs (mean ± SEM) for WTs (filled circles, n = 21) and KOs (open circles, n = 17). Decay of STP was fitted using a bi-exponential decay function (black curve fits WT and grey curve fits KO). The rate of decay of STP1 and STP2 were not significantly different between WTs (τ 1 = 3.0 min, τ2 = 24.0 min) and KOs (τ 1 = 4.7 min, τ2 = 25.8 min) (τ 1 F(1, 3333) = 1.231, p = 0.267, τ 2 F(1, 3333) = 0.0801, p = 0.777, F test). In this and subsequent time course plots, the arrowhead indicates the time of high frequency stimulation and the associated “B” refers to the number of bursts delivered. Representative fEPSPs from WTs and KOs at the time-points indicated in A are shown on the right. (B) The level of STP1 and STP2 were calculated by integrating the fast and slow components of the bi-exponential decay function, respectively, and are presented normalised with respect to the corresponding control. STP1 was significantly lower in WTs (100.0 ± 10.1%) compared to KOs (212.4 ± 19.4%; ****p < 0.0001, t(36) = 5.431, t -test). STP2 was not significantly different between WTs (100.0 ± 13.0%) and KOs (138.7 ± 15.7%; p = 0.0633, t(36) = 1.916, t -test). LTP in WTs (38.5 ± 4.3%) was significantly less than in KOs (52.5 ± 5.5%; t(36) = 2.055, *p = 0.0472, t -test) (C) Time course of potentiation in WTs (filled circles, n = 4) and KOs (open circles, n = 5) in the presence of GABA A and GABA B receptor antagonists. Decay time constant of STP1 and STP2 were not different between WTs (τ 1 = 1.7 min, τ 2 = 19.2 min) and KOs (τ 1 = 2.1 min, τ 2 = 25.1 min; τ 1 F(1, 796) = 1.081, p = 0.299; τ 2 F(1, 796) = 1.172, p = 0.279, F test). In this and subsequent figures, horizontal bars on the time course plots indicates the duration of compound application. (D) STP1 level was significantly lower in WT (100 ± 8.8%) compared to KOs (191.6 ± 32.2%; *p = 0.0437, t(7) = 2.456, t -test). STP2 was significantly greater in WTs (100 ± 13.4%) compared to KOs (45.5 ± 14.5%; *p = 0.0309, t(7) = 2.694, t -test). LTP was similar in WTs (79.4 ± 8.1%) and KOs (67.4 ± 10.7%; t(7) = 0.8548, p = 0.421; t -test).

Article Snippet: The global GluN2D KO mice were obtained from Professor Masayoshi Mishina (University of Kyoto) and maintained at a breeding facility in the UK (Charles River).

Techniques: Control

Enhanced STP and LTP in GluN2D KOs is NMDAR-dependent. (A) Time course of STP and LTP by 10-bursts in WTs. Data from control experiments (Ctrl, black circles, n = 8), 100 μM D-AP5 (red circles, n = 5) and 10 μM L-689,560 (blue circles, n = 3) are shown. (B) Summary of STP1, STP2 and LTP in WTs (from experiments shown in A) from control (STP1 = 100.0 ± 12.3%, STP2 = 100.0 ± 17.5%, LTP = 40.2 ± 8.0%), D-AP5 (STP1 = 3.1 ± 3.1%, STP2 = 50.3 ± 12.0%, LTP = 5.4 ± 2.4%) and L-689,560 (STP1 = 7.4 ± 7.4%, STP2 = 20.7 ± 10.5%, LTP = 2.0 ± 1.1%). STP1 was inhibited by D-AP5 (t(13) = 6.475, ****p < 0.0001, ANOVA with Bonferroni test for multiple comparisons (BT)) and L-689,560 (t(13) = 5.208, ***p = 0.0003, ANOVA with BT). STP2 was not significantly different in the D-AP5 (t(13) = 2.193, p = 0.0941, ANOVA) group but was significantly reduced in L-689,560 (t(13) = 2.945, *p = 0.0227, ANOVA with BT), compared to control. LTP was inhibited by D-AP5 (t(13) = 3.607, **p = 0.0064, ANOVA with BT) and L-689,560 (t(13) = 3.332, *p = 0.0108, ANOVA with BT). (C) Similar to A, but data are from KOs. Interleaved controls (grey circles, n = 8), D-AP5 (red circles, n = 6), and L-689,560 (blue circles, n = 4). (D) Summary of STP and LTP in KOs (from experiments shown in C) from control (STP1 = 100.0 ± 18.2%, STP2 = 100.0 ± 21.1%, LTP = 47.9 ± 8.8%), D-AP5 (STP1 = 17.9 ± 9.8%, STP2 = 34.1 ± 11.0%, LTP = 7.1 ± 3.0%) and L-689,560 (STP1 = 12.2 ± 3.3%, STP2 = 7.6 ± 2.7%, LTP = 5.2 ± 1.4%) experiments. STP1 was inhibited by D-AP5 (t(15) = 4.003, **p = 0.0023, ANOVA with BT) and L-689,560 (t(15) = 3.776, **p = 0.0037, ANOVA with BT). STP2 was inhibited by D-AP5 (t(15) = 2.791, *p = 0.0274, ANOVA with BT) and L-689,560 (t(10) = 3.451, **p = 0.007, ANOVA with BT), compared to control. LTP was inhibited by D-AP5 (t(15) = 4.280, **p = 0.0013, ANOVA with BT) and L-689,560 (t(15) = 3.956, **p = 0.0025, ANOVA with BT) compared to control.

Journal: Neuropharmacology

Article Title: Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

doi: 10.1016/j.neuropharm.2021.108833

Figure Lengend Snippet: Enhanced STP and LTP in GluN2D KOs is NMDAR-dependent. (A) Time course of STP and LTP by 10-bursts in WTs. Data from control experiments (Ctrl, black circles, n = 8), 100 μM D-AP5 (red circles, n = 5) and 10 μM L-689,560 (blue circles, n = 3) are shown. (B) Summary of STP1, STP2 and LTP in WTs (from experiments shown in A) from control (STP1 = 100.0 ± 12.3%, STP2 = 100.0 ± 17.5%, LTP = 40.2 ± 8.0%), D-AP5 (STP1 = 3.1 ± 3.1%, STP2 = 50.3 ± 12.0%, LTP = 5.4 ± 2.4%) and L-689,560 (STP1 = 7.4 ± 7.4%, STP2 = 20.7 ± 10.5%, LTP = 2.0 ± 1.1%). STP1 was inhibited by D-AP5 (t(13) = 6.475, ****p < 0.0001, ANOVA with Bonferroni test for multiple comparisons (BT)) and L-689,560 (t(13) = 5.208, ***p = 0.0003, ANOVA with BT). STP2 was not significantly different in the D-AP5 (t(13) = 2.193, p = 0.0941, ANOVA) group but was significantly reduced in L-689,560 (t(13) = 2.945, *p = 0.0227, ANOVA with BT), compared to control. LTP was inhibited by D-AP5 (t(13) = 3.607, **p = 0.0064, ANOVA with BT) and L-689,560 (t(13) = 3.332, *p = 0.0108, ANOVA with BT). (C) Similar to A, but data are from KOs. Interleaved controls (grey circles, n = 8), D-AP5 (red circles, n = 6), and L-689,560 (blue circles, n = 4). (D) Summary of STP and LTP in KOs (from experiments shown in C) from control (STP1 = 100.0 ± 18.2%, STP2 = 100.0 ± 21.1%, LTP = 47.9 ± 8.8%), D-AP5 (STP1 = 17.9 ± 9.8%, STP2 = 34.1 ± 11.0%, LTP = 7.1 ± 3.0%) and L-689,560 (STP1 = 12.2 ± 3.3%, STP2 = 7.6 ± 2.7%, LTP = 5.2 ± 1.4%) experiments. STP1 was inhibited by D-AP5 (t(15) = 4.003, **p = 0.0023, ANOVA with BT) and L-689,560 (t(15) = 3.776, **p = 0.0037, ANOVA with BT). STP2 was inhibited by D-AP5 (t(15) = 2.791, *p = 0.0274, ANOVA with BT) and L-689,560 (t(10) = 3.451, **p = 0.007, ANOVA with BT), compared to control. LTP was inhibited by D-AP5 (t(15) = 4.280, **p = 0.0013, ANOVA with BT) and L-689,560 (t(15) = 3.956, **p = 0.0025, ANOVA with BT) compared to control.

Article Snippet: The global GluN2D KO mice were obtained from Professor Masayoshi Mishina (University of Kyoto) and maintained at a breeding facility in the UK (Charles River).

Techniques: Control

UBP145 partially inhibits LTP in WTs but has no effect in GluN2D KOs. (A) Time course of potentiation induced by 10-bursts in the presence of GluN2D antagonist 10 μM UBP145 (green circles, n = 7) compared to controls (black circles, n = 7) in WTs. (B) Summary of STP1, STP2 and LTP in WTs (from experiments shown in A) in control (STP1 = 100.0 ± 12.0%, STP2 = 100.0 ± 18.4%, LTP = 47.5 ± 8.3%) and UBP145 experiments (STP1 = 91.6 ± 18.4%, STP2 = 61.6 ± 20.3%, LTP = 23.1 ± 6.5%) in WTs. STP1 was not significantly different between the control and UBP145 groups (t(12) = 0.3813, p = 0.7096, t -test). STP2 was not significantly different between control and UBP145 (t(12) = 1.401, p = 0.1864, t -test). LTP was significantly reduced in UBP145-treated group compared to control (t(12) = 2.314, *p = 0.0392, t -test). (C) GluN2D KOs treated with UBP145 (green circles, n = 8) and controls (grey circles, n = 8). (D) Summary of potentiation in control (STP1 = 100.0 ± 15.8%, STP2 = 100.0 ± 12.4%, LTP = 46.8 ± 9.1%) and UBP145 experiments (STP1 = 71.8 ± 11.1%, STP2 = 83.8 ± 25.6%, LTP = 44.4 ± 7.5%) in KOs. STP1, STP2 and LTP were not significantly different between the control and UBP145 groups in KOs (STP1: t(14) = 1.458, p = 0.1668, t -test; STP2: t(14) = 0.5712, p = 0.5769, t -test; LTP: t(14) = 0.2077, p = 0.8384, t -test).

Journal: Neuropharmacology

Article Title: Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

doi: 10.1016/j.neuropharm.2021.108833

Figure Lengend Snippet: UBP145 partially inhibits LTP in WTs but has no effect in GluN2D KOs. (A) Time course of potentiation induced by 10-bursts in the presence of GluN2D antagonist 10 μM UBP145 (green circles, n = 7) compared to controls (black circles, n = 7) in WTs. (B) Summary of STP1, STP2 and LTP in WTs (from experiments shown in A) in control (STP1 = 100.0 ± 12.0%, STP2 = 100.0 ± 18.4%, LTP = 47.5 ± 8.3%) and UBP145 experiments (STP1 = 91.6 ± 18.4%, STP2 = 61.6 ± 20.3%, LTP = 23.1 ± 6.5%) in WTs. STP1 was not significantly different between the control and UBP145 groups (t(12) = 0.3813, p = 0.7096, t -test). STP2 was not significantly different between control and UBP145 (t(12) = 1.401, p = 0.1864, t -test). LTP was significantly reduced in UBP145-treated group compared to control (t(12) = 2.314, *p = 0.0392, t -test). (C) GluN2D KOs treated with UBP145 (green circles, n = 8) and controls (grey circles, n = 8). (D) Summary of potentiation in control (STP1 = 100.0 ± 15.8%, STP2 = 100.0 ± 12.4%, LTP = 46.8 ± 9.1%) and UBP145 experiments (STP1 = 71.8 ± 11.1%, STP2 = 83.8 ± 25.6%, LTP = 44.4 ± 7.5%) in KOs. STP1, STP2 and LTP were not significantly different between the control and UBP145 groups in KOs (STP1: t(14) = 1.458, p = 0.1668, t -test; STP2: t(14) = 0.5712, p = 0.5769, t -test; LTP: t(14) = 0.2077, p = 0.8384, t -test).

Article Snippet: The global GluN2D KO mice were obtained from Professor Masayoshi Mishina (University of Kyoto) and maintained at a breeding facility in the UK (Charles River).

Techniques: Control

The GluN2D subunit contributes to STP2 and LTP. (A) Time course of potentiation in WTs induced by 30B in controls (purple symbols, n = 4), or in the presence of 10 μM UBP145 (green symbols, n = 4). (B) Summary of STP1, STP2 and LTP in WTs (from experiments shown in A) in control (STP1 = 100.0 ± 31.0%, STP2 = 100.0 ± 17.2%, LTP = 84.3 ± 10.7%) and UBP145 (STP1 = 92.9 ± 27.8%, STP2 = 30.6 ± 18.0%, LTP = 48.5 ± 10.0%) experiments in WTs. STP1 was not significantly different in UBP145 (t(6) = 0.1719, p = 0.8692, t -test) compared to control. STP2 was significantly lower in UBP145 (t(6) = 2.793, *p = 0.0315, t -test). LTP was partially inhibited by UBP145 (t(6) = 3.405, *p = 0.0144, t -test). (C) Equivalent data from KOs. Potentiation of control KOs (purple symbols, n = 6), UBP145 (green symbols, n = 6). (D) Summary of potentiation in control (STP1 = 100.0 ± 31.0%, STP2 = 100.0 ± 9.0%, LTP = 56.8 ± 6.0%), UBP145 (STP1 = 134.4 ± 35.4%, STP2 = 89.4 ± 16.0%, LTP = 51.3 ± 7.7%). STP1, STP2 and LTP were not significantly different upon treatment with UBP145 (STP1: t(10) = 0.732, p = 0.4811, STP2: t(10) = 0.575, p = 0.5781, LTP t(10) = 0.561, p = 0.5869, t -test).

Journal: Neuropharmacology

Article Title: Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

doi: 10.1016/j.neuropharm.2021.108833

Figure Lengend Snippet: The GluN2D subunit contributes to STP2 and LTP. (A) Time course of potentiation in WTs induced by 30B in controls (purple symbols, n = 4), or in the presence of 10 μM UBP145 (green symbols, n = 4). (B) Summary of STP1, STP2 and LTP in WTs (from experiments shown in A) in control (STP1 = 100.0 ± 31.0%, STP2 = 100.0 ± 17.2%, LTP = 84.3 ± 10.7%) and UBP145 (STP1 = 92.9 ± 27.8%, STP2 = 30.6 ± 18.0%, LTP = 48.5 ± 10.0%) experiments in WTs. STP1 was not significantly different in UBP145 (t(6) = 0.1719, p = 0.8692, t -test) compared to control. STP2 was significantly lower in UBP145 (t(6) = 2.793, *p = 0.0315, t -test). LTP was partially inhibited by UBP145 (t(6) = 3.405, *p = 0.0144, t -test). (C) Equivalent data from KOs. Potentiation of control KOs (purple symbols, n = 6), UBP145 (green symbols, n = 6). (D) Summary of potentiation in control (STP1 = 100.0 ± 31.0%, STP2 = 100.0 ± 9.0%, LTP = 56.8 ± 6.0%), UBP145 (STP1 = 134.4 ± 35.4%, STP2 = 89.4 ± 16.0%, LTP = 51.3 ± 7.7%). STP1, STP2 and LTP were not significantly different upon treatment with UBP145 (STP1: t(10) = 0.732, p = 0.4811, STP2: t(10) = 0.575, p = 0.5781, LTP t(10) = 0.561, p = 0.5869, t -test).

Article Snippet: The global GluN2D KO mice were obtained from Professor Masayoshi Mishina (University of Kyoto) and maintained at a breeding facility in the UK (Charles River).

Techniques: Control