nmda receptor antagonist cpp Search Results


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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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Tocris nmda receptor antagonist
a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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Tocris cpp nmda receptor antagonist tocris cat no 0247
a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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Tocris glutamate receptor blockers
a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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Tocris acsf solution
a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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(a) Plot of number of mEPSCs versus membrane capacitance. Cells were classified as NG2+ cells, Pre-OLs or OLs based on DsRed fluorescence, membrane capacitance, membrane resistance, and NaV current density. (b) Graph in a colored according to whether NaV current was detected, showing the tight correlation between loss of synapses and loss of NaV current. (c) HS-response of cells indicated by numbers in a and b. (d) Response of a representative NG2+ cell to glutamate uncaging (black dot), recorded at −80 mV and 40 mV (in NBQX/GYKI53655). (e) Response of a representative Pre-OL to glutamate uncaging at −80 mV and 40 mV (in NBQX/GYKI53655). (f) Response of representative OLs to glutamate uncaging recorded at −80 mV showing effects of NBQX/GYKI53655, RS-CPP (upper trace, 0 <t>Mg++ACSF/3</t> μm D-serine), and TBOA (lower trace, normal ACSF); Insets show initial response at faster time scale (bar = 20 ms). (g) Quantification of peak AMPAR current normalized to membrane capacitance for NG2+ cells (n = 8), Pre-OLs (n=8), and OLs (n = 13); red asterisk: NG2+ cell vs. Pre-OL and NG2+ cell vs. OL, P < 0.001; blue asterisk: OL vs. Pre-OL, P < 0.001.
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(a) Plot of number of mEPSCs versus membrane capacitance. Cells were classified as NG2+ cells, Pre-OLs or OLs based on DsRed fluorescence, membrane capacitance, membrane resistance, and NaV current density. (b) Graph in a colored according to whether NaV current was detected, showing the tight correlation between loss of synapses and loss of NaV current. (c) HS-response of cells indicated by numbers in a and b. (d) Response of a representative NG2+ cell to glutamate uncaging (black dot), recorded at −80 mV and 40 mV (in NBQX/GYKI53655). (e) Response of a representative Pre-OL to glutamate uncaging at −80 mV and 40 mV (in NBQX/GYKI53655). (f) Response of representative OLs to glutamate uncaging recorded at −80 mV showing effects of NBQX/GYKI53655, RS-CPP (upper trace, 0 <t>Mg++ACSF/3</t> μm D-serine), and TBOA (lower trace, normal ACSF); Insets show initial response at faster time scale (bar = 20 ms). (g) Quantification of peak AMPAR current normalized to membrane capacitance for NG2+ cells (n = 8), Pre-OLs (n=8), and OLs (n = 13); red asterisk: NG2+ cell vs. Pre-OL and NG2+ cell vs. OL, P < 0.001; blue asterisk: OL vs. Pre-OL, P < 0.001.
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cpp  (Tocris)
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Tocris cpp
(a) Plot of number of mEPSCs versus membrane capacitance. Cells were classified as NG2+ cells, Pre-OLs or OLs based on DsRed fluorescence, membrane capacitance, membrane resistance, and NaV current density. (b) Graph in a colored according to whether NaV current was detected, showing the tight correlation between loss of synapses and loss of NaV current. (c) HS-response of cells indicated by numbers in a and b. (d) Response of a representative NG2+ cell to glutamate uncaging (black dot), recorded at −80 mV and 40 mV (in NBQX/GYKI53655). (e) Response of a representative Pre-OL to glutamate uncaging at −80 mV and 40 mV (in NBQX/GYKI53655). (f) Response of representative OLs to glutamate uncaging recorded at −80 mV showing effects of NBQX/GYKI53655, RS-CPP (upper trace, 0 <t>Mg++ACSF/3</t> μm D-serine), and TBOA (lower trace, normal ACSF); Insets show initial response at faster time scale (bar = 20 ms). (g) Quantification of peak AMPAR current normalized to membrane capacitance for NG2+ cells (n = 8), Pre-OLs (n=8), and OLs (n = 13); red asterisk: NG2+ cell vs. Pre-OL and NG2+ cell vs. OL, P < 0.001; blue asterisk: OL vs. Pre-OL, P < 0.001.
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Image Search Results


a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D for AMPA and NMDA receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.

Journal: bioRxiv

Article Title: Graded heterogeneity of metabotropic signaling underlies a continuum of cell-intrinsic temporal responses

doi: 10.1101/2020.12.27.424473

Figure Lengend Snippet: a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D for AMPA and NMDA receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.

Article Snippet: Sequential drug wash-ins were performed using a computer-controlled solenoid manifold system (ValveLink 8.2, Automate Scientific, Inc., Berkeley, CA) with a flow rate of 1 to 2mL/min, where indicated, with mGluR1 antagonist (100μM LY357385, Tocris Bio-Techne, Minneapolis, MN), AMPA receptor blocker (5μM NBQX), NMDA receptor blocker (2 μM R-CPP), mGluR2/3 antagonist (1μM LY341495, Tocris Bio-Techne, Minneapolis, MN) and DGK inhibitor II (100 μM R59949, MilliporeSigma, St. Louis, MO)

Techniques: Expressing

a. Examples of instantaneous firing rate from on-cell recordings before (black) and after (gray) the application of AMPA/NMDA receptor antagonist (gray bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. b. Summary of evoked spiking (20×100 Hz) and the effect of AMPA/NMDA receptor antagonist (normalized to baseline, mean±sem, n=5). c. Examples of instantaneous firing rate from on-cell recordings before (black) and after (red) the application of an mGluR1 antagonist (red bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. d. Summary of evoked spiking (20×100 Hz) and the effect of an mGluR1 antagonist (normalized to baseline, mean±sem, n=5). e. Example of instantaneous firing rate before and after 20 minutes of DGK inhibitor II wash-in. f. Summary of half-decay time of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6) g. Summary of peak amplitude of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6)

Journal: bioRxiv

Article Title: Graded heterogeneity of metabotropic signaling underlies a continuum of cell-intrinsic temporal responses

doi: 10.1101/2020.12.27.424473

Figure Lengend Snippet: a. Examples of instantaneous firing rate from on-cell recordings before (black) and after (gray) the application of AMPA/NMDA receptor antagonist (gray bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. b. Summary of evoked spiking (20×100 Hz) and the effect of AMPA/NMDA receptor antagonist (normalized to baseline, mean±sem, n=5). c. Examples of instantaneous firing rate from on-cell recordings before (black) and after (red) the application of an mGluR1 antagonist (red bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. d. Summary of evoked spiking (20×100 Hz) and the effect of an mGluR1 antagonist (normalized to baseline, mean±sem, n=5). e. Example of instantaneous firing rate before and after 20 minutes of DGK inhibitor II wash-in. f. Summary of half-decay time of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6) g. Summary of peak amplitude of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6)

Article Snippet: Sequential drug wash-ins were performed using a computer-controlled solenoid manifold system (ValveLink 8.2, Automate Scientific, Inc., Berkeley, CA) with a flow rate of 1 to 2mL/min, where indicated, with mGluR1 antagonist (100μM LY357385, Tocris Bio-Techne, Minneapolis, MN), AMPA receptor blocker (5μM NBQX), NMDA receptor blocker (2 μM R-CPP), mGluR2/3 antagonist (1μM LY341495, Tocris Bio-Techne, Minneapolis, MN) and DGK inhibitor II (100 μM R59949, MilliporeSigma, St. Louis, MO)

Techniques:

a. Sample cell-attached recording (top) instantaneous firing rate (middle) and synaptic current measured with whole-cell voltage clamp (bottom) in a cell with fast response. b. Same as in A but for a cell with intermediate speed response c. Same as in A but for a cell with clear biphasic synaptic current (bottom) d. Same as in A but for a cell with slow biphasic response e. Same as in A but for a cell with only a pause in firing f. Half-decay times of firing rates vs. half-decay times of currents and linear fit on a log-log plot (R adj 2 = 0.91, slope = 0.88, intercept = -0.22, n = 17) g. Peak firing rate vs. peak current amplitude and linear fit on a log-log plot (R adj 2 = 0.69, slope = 0.71, intercept = -0.65, n = 17) h. Pause duration vs. amplitude of the current at stimulation offset, and linear fit with log 10 response variable (black, R adj 2 = 0.44, slope = 0.01, intercept = -0.42, n = 20) i. Heatmap of peak normalized mGluR1-mediated current (n=10) j. Heatmap of peak normalized mGluR2/3-mediated current (n=7) k. Average synaptic response before (black), after (red) mGluR1 antagonist, and after AMPA/NMDA receptor antagonist wash-ins (grey). Each trace is an average of 8 trials. l. Average synaptic response before (top, black) and after (top, blue) mGluR2/3 antagonist washin, and their difference (bottom, black). Each trace is an average of 8 trials.

Journal: bioRxiv

Article Title: Graded heterogeneity of metabotropic signaling underlies a continuum of cell-intrinsic temporal responses

doi: 10.1101/2020.12.27.424473

Figure Lengend Snippet: a. Sample cell-attached recording (top) instantaneous firing rate (middle) and synaptic current measured with whole-cell voltage clamp (bottom) in a cell with fast response. b. Same as in A but for a cell with intermediate speed response c. Same as in A but for a cell with clear biphasic synaptic current (bottom) d. Same as in A but for a cell with slow biphasic response e. Same as in A but for a cell with only a pause in firing f. Half-decay times of firing rates vs. half-decay times of currents and linear fit on a log-log plot (R adj 2 = 0.91, slope = 0.88, intercept = -0.22, n = 17) g. Peak firing rate vs. peak current amplitude and linear fit on a log-log plot (R adj 2 = 0.69, slope = 0.71, intercept = -0.65, n = 17) h. Pause duration vs. amplitude of the current at stimulation offset, and linear fit with log 10 response variable (black, R adj 2 = 0.44, slope = 0.01, intercept = -0.42, n = 20) i. Heatmap of peak normalized mGluR1-mediated current (n=10) j. Heatmap of peak normalized mGluR2/3-mediated current (n=7) k. Average synaptic response before (black), after (red) mGluR1 antagonist, and after AMPA/NMDA receptor antagonist wash-ins (grey). Each trace is an average of 8 trials. l. Average synaptic response before (top, black) and after (top, blue) mGluR2/3 antagonist washin, and their difference (bottom, black). Each trace is an average of 8 trials.

Article Snippet: Sequential drug wash-ins were performed using a computer-controlled solenoid manifold system (ValveLink 8.2, Automate Scientific, Inc., Berkeley, CA) with a flow rate of 1 to 2mL/min, where indicated, with mGluR1 antagonist (100μM LY357385, Tocris Bio-Techne, Minneapolis, MN), AMPA receptor blocker (5μM NBQX), NMDA receptor blocker (2 μM R-CPP), mGluR2/3 antagonist (1μM LY341495, Tocris Bio-Techne, Minneapolis, MN) and DGK inhibitor II (100 μM R59949, MilliporeSigma, St. Louis, MO)

Techniques:

(a) Plot of number of mEPSCs versus membrane capacitance. Cells were classified as NG2+ cells, Pre-OLs or OLs based on DsRed fluorescence, membrane capacitance, membrane resistance, and NaV current density. (b) Graph in a colored according to whether NaV current was detected, showing the tight correlation between loss of synapses and loss of NaV current. (c) HS-response of cells indicated by numbers in a and b. (d) Response of a representative NG2+ cell to glutamate uncaging (black dot), recorded at −80 mV and 40 mV (in NBQX/GYKI53655). (e) Response of a representative Pre-OL to glutamate uncaging at −80 mV and 40 mV (in NBQX/GYKI53655). (f) Response of representative OLs to glutamate uncaging recorded at −80 mV showing effects of NBQX/GYKI53655, RS-CPP (upper trace, 0 Mg++ACSF/3 μm D-serine), and TBOA (lower trace, normal ACSF); Insets show initial response at faster time scale (bar = 20 ms). (g) Quantification of peak AMPAR current normalized to membrane capacitance for NG2+ cells (n = 8), Pre-OLs (n=8), and OLs (n = 13); red asterisk: NG2+ cell vs. Pre-OL and NG2+ cell vs. OL, P < 0.001; blue asterisk: OL vs. Pre-OL, P < 0.001.

Journal:

Article Title: Excitability and Synaptic Communication within the Oligodendrocyte Lineage

doi: 10.1523/JNEUROSCI.6000-09.2010

Figure Lengend Snippet: (a) Plot of number of mEPSCs versus membrane capacitance. Cells were classified as NG2+ cells, Pre-OLs or OLs based on DsRed fluorescence, membrane capacitance, membrane resistance, and NaV current density. (b) Graph in a colored according to whether NaV current was detected, showing the tight correlation between loss of synapses and loss of NaV current. (c) HS-response of cells indicated by numbers in a and b. (d) Response of a representative NG2+ cell to glutamate uncaging (black dot), recorded at −80 mV and 40 mV (in NBQX/GYKI53655). (e) Response of a representative Pre-OL to glutamate uncaging at −80 mV and 40 mV (in NBQX/GYKI53655). (f) Response of representative OLs to glutamate uncaging recorded at −80 mV showing effects of NBQX/GYKI53655, RS-CPP (upper trace, 0 Mg++ACSF/3 μm D-serine), and TBOA (lower trace, normal ACSF); Insets show initial response at faster time scale (bar = 20 ms). (g) Quantification of peak AMPAR current normalized to membrane capacitance for NG2+ cells (n = 8), Pre-OLs (n=8), and OLs (n = 13); red asterisk: NG2+ cell vs. Pre-OL and NG2+ cell vs. OL, P < 0.001; blue asterisk: OL vs. Pre-OL, P < 0.001.

Article Snippet: The following agents were applied by addition to the superfusing ACSF: TTX (NaV antagonist; Ascent Scientific, 1 μM; gabazine (SR-95531; GABA receptor antagonist; Tocris, 5μM; RS-CPP (NMDA receptor antagonist; Tocris, 5μM or 20 μM for uncaging); 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX; competitive AMPA/kainate receptor antagonist; Tocris, 5 μM or 50 μM for uncaging); GYKI 53655 (AMPA selective, non-competitive antagonist; IVAX 100 μM; TBOA (competitive glutamate transporter blocker; Tocris, 300 μM).

Techniques: Membrane, Fluorescence