tta p2  (Alomone Labs)


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    Structured Review

    Alomone Labs tta p2
    The selective T-type calcium channel inhibitor, <t>TTA-P2,</t> blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro"

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2017.04.002

    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Figure Legend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Techniques Used: Incubation, Blocking Assay, Injection

    2) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    3) Product Images from "Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro"

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2017.04.002

    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Figure Legend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Techniques Used: Incubation, Blocking Assay, Injection

    4) Product Images from "Accumulation of Cav3.2 T-type Calcium Channels in the Uninjured Sural Nerve Contributes to Neuropathic Pain in Rats with Spared Nerve Injury"

    Article Title: Accumulation of Cav3.2 T-type Calcium Channels in the Uninjured Sural Nerve Contributes to Neuropathic Pain in Rats with Spared Nerve Injury

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2018.00024

    Perineural application of mibefradil or TTA-P2 decreased mechanical allodynia at day 14 after SNI. (A,B) Ipsilateral perineural perfusion of mibefradil (1.0 mM, 100 μl) or TTA-P2 (0.5 mM, 100 μl) partially reversed mechanical allodynia in a time-dependent manner. ** p
    Figure Legend Snippet: Perineural application of mibefradil or TTA-P2 decreased mechanical allodynia at day 14 after SNI. (A,B) Ipsilateral perineural perfusion of mibefradil (1.0 mM, 100 μl) or TTA-P2 (0.5 mM, 100 μl) partially reversed mechanical allodynia in a time-dependent manner. ** p

    Techniques Used:

    5) Product Images from "Alterations in Oscillatory Behavior of Central Medial Thalamic Neurons Demonstrate a Key Role of CaV3.1 Isoform of T-Channels During Isoflurane-Induced Anesthesia"

    Article Title: Alterations in Oscillatory Behavior of Central Medial Thalamic Neurons Demonstrate a Key Role of CaV3.1 Isoform of T-Channels During Isoflurane-Induced Anesthesia

    Journal: Cerebral Cortex (New York, NY)

    doi: 10.1093/cercor/bhz002

    Oscillatory differences between WT and Ca V 3.1 KO mice in CeM during TTA-P2 administration in vivo. A , Representative spectrograms from CeM 30 min after i.p. injection of 60 mg/kg TTA-P2 recorded from WT (left) and Ca V 3.1 KO (right) mice. B , Power density and relative power (inset in figure) revealed decreased percentage of δ and increased percentage in α and β waves in Ca V 3.1 KO mice after TTA-P2 (two way RM ANOVA: F (4,60) = 43.87, P
    Figure Legend Snippet: Oscillatory differences between WT and Ca V 3.1 KO mice in CeM during TTA-P2 administration in vivo. A , Representative spectrograms from CeM 30 min after i.p. injection of 60 mg/kg TTA-P2 recorded from WT (left) and Ca V 3.1 KO (right) mice. B , Power density and relative power (inset in figure) revealed decreased percentage of δ and increased percentage in α and β waves in Ca V 3.1 KO mice after TTA-P2 (two way RM ANOVA: F (4,60) = 43.87, P

    Techniques Used: Mouse Assay, In Vivo, Injection

    TTA-P2 reduced tonic and rebound burst firing in CeM neurons from WT mice. A , Original traces from a representative neuron after depolarizing (75 pA) and hyperpolarizing current injection (−25 pA) in the CeM before (left panel, black trace) and after application of TTA-P2 (right panel, gray trace). B , TTA-P2 reduced tonic action potential firing frequency across some current pulses (from 50 to 100 pA) in WT mice (9 cells, 4 animals; two way RM ANOVA: interaction F (6,48) = 5.68, P
    Figure Legend Snippet: TTA-P2 reduced tonic and rebound burst firing in CeM neurons from WT mice. A , Original traces from a representative neuron after depolarizing (75 pA) and hyperpolarizing current injection (−25 pA) in the CeM before (left panel, black trace) and after application of TTA-P2 (right panel, gray trace). B , TTA-P2 reduced tonic action potential firing frequency across some current pulses (from 50 to 100 pA) in WT mice (9 cells, 4 animals; two way RM ANOVA: interaction F (6,48) = 5.68, P

    Techniques Used: Mouse Assay, Injection

    Voltage-dependent T-current inhibition by TTA-P2 in CeM neurons from WT mice. A , Traces of T-current in a representative CeM neuron in control conditions (WT mice) recorded using a double-pulse protocol with 3.6-s-long prepulses to variable voltages (from −120 to −50 mV in 5 mV increment, black); traces from the same cell using the identical voltage-protocol during an apparent steady-state inhibition of T-current in the presence of 5 μM TTA-P2 (gray). B , Average normalized steady-state inactivation ( I / I max ) curves in control conditions and after application of TTA-P2 in the same cells with respective V 50 values. TTA-P2 induced a hyperpolarizing shift in V 50 of 12.5 mV (two tailed unpaired t -test: t (12) = 4.16, P = 0.001). The average V 50 value for steady-state inactivation was −71.5 ± 0.7 mV with slope factor of 4.6 ± 0.6 in control conditions (black, 7 cells, 3 animals). After TTA-P2 perfusion of the same cells, the V 50 value was −84.0 ± 2.9 mV with slope factor of 10.4 ± 3.3 (gray). The slope factor was not significantly different after TTA-P2 perfusion (unpaired two-tailed t -test, t (12) = 1.75, P = 0.106). C , Averaged representative traces recorded under control conditions (black) and after application of TTA-P2 (gray) using a protocol depicted on the top of traces ( V t = −50 mV, V h = −90 mV). D , Averaged normalized current density ( V t = −50 mV, V h = −90 mV) show reduction in current density by 85.36 ± 9.09% (mean ± SD) after application of TTA-P2 (7 cells, 3 animals; two-tailed paired t -test: t (6) = 8.44, P
    Figure Legend Snippet: Voltage-dependent T-current inhibition by TTA-P2 in CeM neurons from WT mice. A , Traces of T-current in a representative CeM neuron in control conditions (WT mice) recorded using a double-pulse protocol with 3.6-s-long prepulses to variable voltages (from −120 to −50 mV in 5 mV increment, black); traces from the same cell using the identical voltage-protocol during an apparent steady-state inhibition of T-current in the presence of 5 μM TTA-P2 (gray). B , Average normalized steady-state inactivation ( I / I max ) curves in control conditions and after application of TTA-P2 in the same cells with respective V 50 values. TTA-P2 induced a hyperpolarizing shift in V 50 of 12.5 mV (two tailed unpaired t -test: t (12) = 4.16, P = 0.001). The average V 50 value for steady-state inactivation was −71.5 ± 0.7 mV with slope factor of 4.6 ± 0.6 in control conditions (black, 7 cells, 3 animals). After TTA-P2 perfusion of the same cells, the V 50 value was −84.0 ± 2.9 mV with slope factor of 10.4 ± 3.3 (gray). The slope factor was not significantly different after TTA-P2 perfusion (unpaired two-tailed t -test, t (12) = 1.75, P = 0.106). C , Averaged representative traces recorded under control conditions (black) and after application of TTA-P2 (gray) using a protocol depicted on the top of traces ( V t = −50 mV, V h = −90 mV). D , Averaged normalized current density ( V t = −50 mV, V h = −90 mV) show reduction in current density by 85.36 ± 9.09% (mean ± SD) after application of TTA-P2 (7 cells, 3 animals; two-tailed paired t -test: t (6) = 8.44, P

    Techniques Used: Inhibition, Mouse Assay, Two Tailed Test

    6) Product Images from "Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability"

    Article Title: Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability

    Journal: Frontiers in Neural Circuits

    doi: 10.3389/fncir.2021.778022

    Selective ligands of T-type calcium channels inhibit cholinergic gamma oscillations in rat hippocampal slices. (A) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (purple) application of the selective T-type calcium channel blocker TTA-P2 (1 μM). (B) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (red) application of the selective T-type calcium channel enhancer SAK3 (0.1 μM). (C) Normalized power before, during and after bath application (gray) of the selective T-type blocker TTA-P2 (1 μM, purple) and NNC55-0396 (100 μM, orange) compared to control (blue). (D) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the power of hippocampal gamma oscillations compared to time matched and solvent control. Control (light blue): n = 13 slices, N = 9 animals; TTA-P2 (1 μM, purple): n = 14, N = 6, p = 0.005, NNC55-0396 (100 μM, orange): n = 6, N = 2, p = 0.001; DMSO control (dark blue): n = 8, N = 7; SAK3 (0.1 μM, red): n = 10, N = 6, p = 0.020. (E) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the peak frequency of hippocampal gamma oscillations compared to time matched and solvent control. TTA-P2 (1 μM, purple): p = 0.042; NNC55-0396 (100 μM, orange): p = 0.001; SAK3 (0.1 μM, red): p = 0.306. Recording temperature was between 34 and 36°C. Traces were lowpass filtered at 200 Hz and bandstop filtered at 50 Hz. Bars show mean ± SEM. * p
    Figure Legend Snippet: Selective ligands of T-type calcium channels inhibit cholinergic gamma oscillations in rat hippocampal slices. (A) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (purple) application of the selective T-type calcium channel blocker TTA-P2 (1 μM). (B) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (red) application of the selective T-type calcium channel enhancer SAK3 (0.1 μM). (C) Normalized power before, during and after bath application (gray) of the selective T-type blocker TTA-P2 (1 μM, purple) and NNC55-0396 (100 μM, orange) compared to control (blue). (D) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the power of hippocampal gamma oscillations compared to time matched and solvent control. Control (light blue): n = 13 slices, N = 9 animals; TTA-P2 (1 μM, purple): n = 14, N = 6, p = 0.005, NNC55-0396 (100 μM, orange): n = 6, N = 2, p = 0.001; DMSO control (dark blue): n = 8, N = 7; SAK3 (0.1 μM, red): n = 10, N = 6, p = 0.020. (E) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the peak frequency of hippocampal gamma oscillations compared to time matched and solvent control. TTA-P2 (1 μM, purple): p = 0.042; NNC55-0396 (100 μM, orange): p = 0.001; SAK3 (0.1 μM, red): p = 0.306. Recording temperature was between 34 and 36°C. Traces were lowpass filtered at 200 Hz and bandstop filtered at 50 Hz. Bars show mean ± SEM. * p

    Techniques Used:

    7) Product Images from "Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord"

    Article Title: Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00370

    Effect of T-type calcium channel blockers on the intrinsic membrane properties of SG neurons. (A) Representative T-type current traces in response to voltage-clamp protocol shown below traces in the treatment of control (black) and TTA-P2 (red). (B) Population data showing the peak amplitude of T-type currents in the absence (black) and presence of TTA-P2 (red). (C) Examples of depolarizing and hyperpolarizing traces in response to current-clamp protocols shown below traces before (black) and after (red) the treatment of TTA-P2. (D) Population data showing the rebound depolarization-evoked spike frequency plotted as a function of test potentials in the absence (black) and presence of TTA-P2 (red). (E) Population data showing the AP spike frequency plotted as a function of elicited currents in the absence (black) and presence of TTA-P2 (red). (F) Bar plots showing the various intrinsic membrane properties of SG neurons in the treatment of control (black) and TTA-P2 (red). V membrane : membrane potential measured at I hold = 0. * P
    Figure Legend Snippet: Effect of T-type calcium channel blockers on the intrinsic membrane properties of SG neurons. (A) Representative T-type current traces in response to voltage-clamp protocol shown below traces in the treatment of control (black) and TTA-P2 (red). (B) Population data showing the peak amplitude of T-type currents in the absence (black) and presence of TTA-P2 (red). (C) Examples of depolarizing and hyperpolarizing traces in response to current-clamp protocols shown below traces before (black) and after (red) the treatment of TTA-P2. (D) Population data showing the rebound depolarization-evoked spike frequency plotted as a function of test potentials in the absence (black) and presence of TTA-P2 (red). (E) Population data showing the AP spike frequency plotted as a function of elicited currents in the absence (black) and presence of TTA-P2 (red). (F) Bar plots showing the various intrinsic membrane properties of SG neurons in the treatment of control (black) and TTA-P2 (red). V membrane : membrane potential measured at I hold = 0. * P

    Techniques Used:

    8) Product Images from "L- and T-type calcium channels control aldosterone production from human adrenals"

    Article Title: L- and T-type calcium channels control aldosterone production from human adrenals

    Journal: The Journal of endocrinology

    doi: 10.1530/JOE-19-0259

    Effect of combined exposure to nifedipine and TTA-P2 on the basal production of aldosterone from human adrenal slices. Both nifedipine and TTA-P2 maximally inhibit aldosterone secretion. A, TTA-P2 does not alter nifedipine-induced inhibition of aldosterone production from human adrenal slices. B, Nifedipine does not alter TTA-P2 inhibition of aldosterone production from human adrenal slices (n = 5). C, Effects of different concentrations of nifedipine or TTA-P2 on Ca V 3.2/3 and Ca V 1.2/3 channel currents in H295R cells. D, 100 nm/L nifedipine and 200 nm/L TTA-P2 showed additive effect on basal aldosterone secretion. #, p
    Figure Legend Snippet: Effect of combined exposure to nifedipine and TTA-P2 on the basal production of aldosterone from human adrenal slices. Both nifedipine and TTA-P2 maximally inhibit aldosterone secretion. A, TTA-P2 does not alter nifedipine-induced inhibition of aldosterone production from human adrenal slices. B, Nifedipine does not alter TTA-P2 inhibition of aldosterone production from human adrenal slices (n = 5). C, Effects of different concentrations of nifedipine or TTA-P2 on Ca V 3.2/3 and Ca V 1.2/3 channel currents in H295R cells. D, 100 nm/L nifedipine and 200 nm/L TTA-P2 showed additive effect on basal aldosterone secretion. #, p

    Techniques Used: Inhibition

    Effects of nifedipine (500 nmol/L) or TTA-P2(2 μmol/L) on Ca V 3.2/3 and Ca V 1.2 /3 channel currents in H295R cells. A, Effects of L-type Ca 2+ channel inhibitor nifedipine and T-type Ca 2+ channel inhibitor TTA-P2 on Ca V 3.2 channel currents (n = 6). B, Effects of 500 nmol/L nifedipine and 2 μmol/L TTA-P2 on Ca V 3.3 channel currents(n = 5). C, Effects of 500 nmol/L nifedipine and 2 μmol/L TTA-P2 on Ca V 1.2 channel currents(n = 5). D, Effects of 500 nmol/L nifedipine and 2 μmol/L TTA-P2 on Ca V 1.3 channel currents(n = 5). Calcium currents were elicited by a 50-ms depolarizing pulse to −20 mV from a holding potential of −90 mV at 10 s intervals.
    Figure Legend Snippet: Effects of nifedipine (500 nmol/L) or TTA-P2(2 μmol/L) on Ca V 3.2/3 and Ca V 1.2 /3 channel currents in H295R cells. A, Effects of L-type Ca 2+ channel inhibitor nifedipine and T-type Ca 2+ channel inhibitor TTA-P2 on Ca V 3.2 channel currents (n = 6). B, Effects of 500 nmol/L nifedipine and 2 μmol/L TTA-P2 on Ca V 3.3 channel currents(n = 5). C, Effects of 500 nmol/L nifedipine and 2 μmol/L TTA-P2 on Ca V 1.2 channel currents(n = 5). D, Effects of 500 nmol/L nifedipine and 2 μmol/L TTA-P2 on Ca V 1.3 channel currents(n = 5). Calcium currents were elicited by a 50-ms depolarizing pulse to −20 mV from a holding potential of −90 mV at 10 s intervals.

    Techniques Used:

    Effect of TTA-P2 on Angiotensin II (Ang II) - or high K + - stimulated aldosterone secretion from human adrenal slices. A, TTA-P2 abrogates Ang II-stimulated aldosterone secretion from human adrenal slices. B, Statistical analysis of TTA-P2 induced inhibition of Ang II-stimulated aldosterone secretion. Data are presented as fold over control. *, P
    Figure Legend Snippet: Effect of TTA-P2 on Angiotensin II (Ang II) - or high K + - stimulated aldosterone secretion from human adrenal slices. A, TTA-P2 abrogates Ang II-stimulated aldosterone secretion from human adrenal slices. B, Statistical analysis of TTA-P2 induced inhibition of Ang II-stimulated aldosterone secretion. Data are presented as fold over control. *, P

    Techniques Used: Inhibition

    Effect of combined exposure to nifedipine and TTA-P2 on Ang II or high K + -stimulated aldosterone secretion from human adrenal slices. A, 100 nm/L nifedipine and 200 nm/L TTA-P2 showed additive inhibitory effect on Ang II–stimulated aldosterone secretion from human adrenal slices. #, p
    Figure Legend Snippet: Effect of combined exposure to nifedipine and TTA-P2 on Ang II or high K + -stimulated aldosterone secretion from human adrenal slices. A, 100 nm/L nifedipine and 200 nm/L TTA-P2 showed additive inhibitory effect on Ang II–stimulated aldosterone secretion from human adrenal slices. #, p

    Techniques Used:

    9) Product Images from "Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels) Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels"

    Article Title: Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels) Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.14149

    Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis through a T‐type VGCC sensitive pathway. (A) Representative images showing immunoreactivities to dendritic and synaptic markers in DRG/spinal cord neuron co‐cultures in the presence or absence of TSP4 (20 nM) and with or without indicated VGCC blockers for 4 days. Scale bar = 10 μm. (B) Summarized data showing that only T‐type VGCC blocker TTA‐P2, but not any other VGCC blockers tested, could block Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis. Means ± SEM from 20 neurons per group that were randomly selected from four wells of multiple culture plates of independent experiments. * P
    Figure Legend Snippet: Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis through a T‐type VGCC sensitive pathway. (A) Representative images showing immunoreactivities to dendritic and synaptic markers in DRG/spinal cord neuron co‐cultures in the presence or absence of TSP4 (20 nM) and with or without indicated VGCC blockers for 4 days. Scale bar = 10 μm. (B) Summarized data showing that only T‐type VGCC blocker TTA‐P2, but not any other VGCC blockers tested, could block Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis. Means ± SEM from 20 neurons per group that were randomly selected from four wells of multiple culture plates of independent experiments. * P

    Techniques Used: Blocking Assay

    10) Product Images from "Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of CaV1 channels"

    Article Title: Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of CaV1 channels

    Journal: BMC Neuroscience

    doi: 10.1186/s12868-018-0441-0

    Calcium channels expressed in striatal FSI. a Left: representative time course of peak maximum Ca 2+ current amplitude during the sequential addition of 20 µM nicardipine, a Ca V 1 (L) channel antagonist, 1 µM ω-conotoxin GIVA (ω-CgTx), a Ca V 2.2 (N) channel antagonist, and 1 µM ω-agatoxin TK (ω-AgTx), a Ca V 2.1 (P/Q) channel antagonist. Right: Representative I–V plots obtained during sequential application of each Ca 2+ channel antagonist and the consequent Ca 2+ current reduction. Note remaining unblocked current. b Left: Time course of maximum Ca 2+ current amplitude showing the action of saturating concentrations of 1 µM SNX-482 (SNX), a Ca V 2.3 (R) channel antagonist and 1 µM TTA-P2 (TTA), a Ca V 3 (T) channel antagonist. Right: Representative I–V plots during sequential application of Ca 2+ channel antagonists with the consequent Ca 2+ current reduction. Average percentage of current reduction in a sample of experiments after each channel antagonist was taken as the contribution of a specific Ca 2+ channel class as seen in Table 1
    Figure Legend Snippet: Calcium channels expressed in striatal FSI. a Left: representative time course of peak maximum Ca 2+ current amplitude during the sequential addition of 20 µM nicardipine, a Ca V 1 (L) channel antagonist, 1 µM ω-conotoxin GIVA (ω-CgTx), a Ca V 2.2 (N) channel antagonist, and 1 µM ω-agatoxin TK (ω-AgTx), a Ca V 2.1 (P/Q) channel antagonist. Right: Representative I–V plots obtained during sequential application of each Ca 2+ channel antagonist and the consequent Ca 2+ current reduction. Note remaining unblocked current. b Left: Time course of maximum Ca 2+ current amplitude showing the action of saturating concentrations of 1 µM SNX-482 (SNX), a Ca V 2.3 (R) channel antagonist and 1 µM TTA-P2 (TTA), a Ca V 3 (T) channel antagonist. Right: Representative I–V plots during sequential application of Ca 2+ channel antagonists with the consequent Ca 2+ current reduction. Average percentage of current reduction in a sample of experiments after each channel antagonist was taken as the contribution of a specific Ca 2+ channel class as seen in Table 1

    Techniques Used:

    11) Product Images from "Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord"

    Article Title: Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00370

    Effect of T-type calcium channel blockers on the intrinsic membrane properties of SG neurons. (A) Representative T-type current traces in response to voltage-clamp protocol shown below traces in the treatment of control (black) and TTA-P2 (red). (B) Population data showing the peak amplitude of T-type currents in the absence (black) and presence of TTA-P2 (red). (C) Examples of depolarizing and hyperpolarizing traces in response to current-clamp protocols shown below traces before (black) and after (red) the treatment of TTA-P2. (D) Population data showing the rebound depolarization-evoked spike frequency plotted as a function of test potentials in the absence (black) and presence of TTA-P2 (red). (E) Population data showing the AP spike frequency plotted as a function of elicited currents in the absence (black) and presence of TTA-P2 (red). (F) Bar plots showing the various intrinsic membrane properties of SG neurons in the treatment of control (black) and TTA-P2 (red). V membrane : membrane potential measured at I hold = 0. * P
    Figure Legend Snippet: Effect of T-type calcium channel blockers on the intrinsic membrane properties of SG neurons. (A) Representative T-type current traces in response to voltage-clamp protocol shown below traces in the treatment of control (black) and TTA-P2 (red). (B) Population data showing the peak amplitude of T-type currents in the absence (black) and presence of TTA-P2 (red). (C) Examples of depolarizing and hyperpolarizing traces in response to current-clamp protocols shown below traces before (black) and after (red) the treatment of TTA-P2. (D) Population data showing the rebound depolarization-evoked spike frequency plotted as a function of test potentials in the absence (black) and presence of TTA-P2 (red). (E) Population data showing the AP spike frequency plotted as a function of elicited currents in the absence (black) and presence of TTA-P2 (red). (F) Bar plots showing the various intrinsic membrane properties of SG neurons in the treatment of control (black) and TTA-P2 (red). V membrane : membrane potential measured at I hold = 0. * P

    Techniques Used:

    12) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    13) Product Images from "Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels) Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels"

    Article Title: Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels) Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.14149

    Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis through a T‐type VGCC sensitive pathway. (A) Representative images showing immunoreactivities to dendritic and synaptic markers in DRG/spinal cord neuron co‐cultures in the presence or absence of TSP4 (20 nM) and with or without indicated VGCC blockers for 4 days. Scale bar = 10 μm. (B) Summarized data showing that only T‐type VGCC blocker TTA‐P2, but not any other VGCC blockers tested, could block Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis. Means ± SEM from 20 neurons per group that were randomly selected from four wells of multiple culture plates of independent experiments. * P
    Figure Legend Snippet: Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis through a T‐type VGCC sensitive pathway. (A) Representative images showing immunoreactivities to dendritic and synaptic markers in DRG/spinal cord neuron co‐cultures in the presence or absence of TSP4 (20 nM) and with or without indicated VGCC blockers for 4 days. Scale bar = 10 μm. (B) Summarized data showing that only T‐type VGCC blocker TTA‐P2, but not any other VGCC blockers tested, could block Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis. Means ± SEM from 20 neurons per group that were randomly selected from four wells of multiple culture plates of independent experiments. * P

    Techniques Used: Blocking Assay

    14) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    15) Product Images from "TRPM4 conductances in thalamic reticular nucleus neurons generate persistent firing during slow oscillations"

    Article Title: TRPM4 conductances in thalamic reticular nucleus neurons generate persistent firing during slow oscillations

    Journal: bioRxiv

    doi: 10.1101/2020.02.11.943746

    T-type Ca 2+ channels but not mGluRs are required for PF. A. Representative recordings of PF from two different TRN neurons, in control conditions and in the presence of the mGluR1 antagonist JNJ 16259685 (1 µM) and the mGluR5 antagonist MTEP (10 µM). B. Summary data quantifying duration of evoked membrane depolarization in control (n = 111) and in the presence of mGluR 1/5 antagonists (n = 23). C. Representative recording of neuron with PF, initially held at a holding potential of -60 mV and then at -75 mV. D. Summary data quantifying evoked depolarization duration as a function of holding potential (n = 15 TRN neurons). E. Representative recordings in the presence of apamin and in the presence of apamin and the T-type Ca 2+ channel antagonist TTA-P2 (1 µM). F. Summary data quantifying evoked depolarization duration (n = 50 in apamin, n = 17 in apamin + TTA-P2).
    Figure Legend Snippet: T-type Ca 2+ channels but not mGluRs are required for PF. A. Representative recordings of PF from two different TRN neurons, in control conditions and in the presence of the mGluR1 antagonist JNJ 16259685 (1 µM) and the mGluR5 antagonist MTEP (10 µM). B. Summary data quantifying duration of evoked membrane depolarization in control (n = 111) and in the presence of mGluR 1/5 antagonists (n = 23). C. Representative recording of neuron with PF, initially held at a holding potential of -60 mV and then at -75 mV. D. Summary data quantifying evoked depolarization duration as a function of holding potential (n = 15 TRN neurons). E. Representative recordings in the presence of apamin and in the presence of apamin and the T-type Ca 2+ channel antagonist TTA-P2 (1 µM). F. Summary data quantifying evoked depolarization duration (n = 50 in apamin, n = 17 in apamin + TTA-P2).

    Techniques Used:

    16) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    17) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    18) Product Images from "Global genetic deletion of CaV3.3 channels facilitates anaesthetic induction and enhances isoflurane-sparing effects of T-type calcium channel blockers"

    Article Title: Global genetic deletion of CaV3.3 channels facilitates anaesthetic induction and enhances isoflurane-sparing effects of T-type calcium channel blockers

    Journal: Scientific Reports

    doi: 10.1038/s41598-020-78488-8

    Selective pharmacological inhibition of T-channels with TTA-P2 facilitates anesthetic induction with isoflurane in the WT and mutant mice. Both WT and Ca V 3.3 KO mice were injected with vehicle first (data from Fig. 1 A) or TTA-P2 on different day and placed in a chamber set at 1.2% isoflurane after a 30-min wait period. Successful induction was determined when a mouse failed to right within a 30-s period. Note that both cohorts demonstrated a significant treatment difference (two-way RM ANOVA: F 1,17 = 127.40, p
    Figure Legend Snippet: Selective pharmacological inhibition of T-channels with TTA-P2 facilitates anesthetic induction with isoflurane in the WT and mutant mice. Both WT and Ca V 3.3 KO mice were injected with vehicle first (data from Fig. 1 A) or TTA-P2 on different day and placed in a chamber set at 1.2% isoflurane after a 30-min wait period. Successful induction was determined when a mouse failed to right within a 30-s period. Note that both cohorts demonstrated a significant treatment difference (two-way RM ANOVA: F 1,17 = 127.40, p

    Techniques Used: Inhibition, Mutagenesis, Mouse Assay, Injection

    Dose-dependent sparing effect of TTA-P2 on isoflurane-induced hypnosis in the mutant and WT mice. ( A ) Percent isoflurane at LORR for WT mice. Data from WT mice injected with vehicle in Fig. 1 B is used here as baseline. WT mice have a dose dependent decrease in the % isoflurane as the dose of TTA-P2 was escalated (one-way ANOVA: F 3,36 = 29.14, p
    Figure Legend Snippet: Dose-dependent sparing effect of TTA-P2 on isoflurane-induced hypnosis in the mutant and WT mice. ( A ) Percent isoflurane at LORR for WT mice. Data from WT mice injected with vehicle in Fig. 1 B is used here as baseline. WT mice have a dose dependent decrease in the % isoflurane as the dose of TTA-P2 was escalated (one-way ANOVA: F 3,36 = 29.14, p

    Techniques Used: Mutagenesis, Mouse Assay, Injection

    Oscillatory differences between the WT and Ca V 3.3 KO mice pretreated with TTA-P2 during administration of sub-hypnotic concentrations of isoflurane. ( A ) Representative EEG traces and heat maps from a WT mouse (upper panel) and a Ca V 3.3 KO mouse (lower panel) during administration of 0.6% isoflurane (ISO) following pretreatment with TTA-P2 at 60 mg/kg i.p. ( B ) Analysis of total power showed a rise in slow frequency range (δ and θ range) in the mutant mice in comparison with the WT group (two-way RM ANOVA: Interaction F 4,56 = 4.11, p = 0.005, Frequency F 4,56 = 137.40, p
    Figure Legend Snippet: Oscillatory differences between the WT and Ca V 3.3 KO mice pretreated with TTA-P2 during administration of sub-hypnotic concentrations of isoflurane. ( A ) Representative EEG traces and heat maps from a WT mouse (upper panel) and a Ca V 3.3 KO mouse (lower panel) during administration of 0.6% isoflurane (ISO) following pretreatment with TTA-P2 at 60 mg/kg i.p. ( B ) Analysis of total power showed a rise in slow frequency range (δ and θ range) in the mutant mice in comparison with the WT group (two-way RM ANOVA: Interaction F 4,56 = 4.11, p = 0.005, Frequency F 4,56 = 137.40, p

    Techniques Used: Mouse Assay, Mutagenesis

    Isoflurane-sparing effect of anaesthetic hypnosis for TTA-P2 is more prominent in the Ca V 3.3 KO mice than in the WT and Ca V 3.1 KO mice. The Ca V 3.3 KO mice pretreated with TTA-P2 required a significantly lower concentration of isoflurane compared to the WT mice at 10 mg/kg and 60 mg/kg of TTA-P2 for each genotype (two-way RM ANOVA: Interaction F 6,81 = 2.53, p = 0.005, Dose F 3,76 = 127.40, p
    Figure Legend Snippet: Isoflurane-sparing effect of anaesthetic hypnosis for TTA-P2 is more prominent in the Ca V 3.3 KO mice than in the WT and Ca V 3.1 KO mice. The Ca V 3.3 KO mice pretreated with TTA-P2 required a significantly lower concentration of isoflurane compared to the WT mice at 10 mg/kg and 60 mg/kg of TTA-P2 for each genotype (two-way RM ANOVA: Interaction F 6,81 = 2.53, p = 0.005, Dose F 3,76 = 127.40, p

    Techniques Used: Mouse Assay, Concentration Assay

    19) Product Images from "Cytosolic ATP Relieves Voltage-Dependent Inactivation of T-Type Calcium Channels and Facilitates Excitability of Neurons in the Rat Central Medial Thalamus"

    Article Title: Cytosolic ATP Relieves Voltage-Dependent Inactivation of T-Type Calcium Channels and Facilitates Excitability of Neurons in the Rat Central Medial Thalamus

    Journal: eNeuro

    doi: 10.1523/ENEURO.0016-18.2018

    TTA-P2 reduced tonic and rebound burst firing in CeM neurons. A , Original traces from a representative neuron in the CeM before application of TTA-P2 (left panel, orange trace), after application of TTA-P2 (middle panel, violet trace) and after wash (right panel, orange trace). Resting membrane potentials (shown in the lower left corner of each panel) show active membrane responses to a depolarizing (100 pA) current injection. B , TTA-P2 reduced tonic AP firing frequency across all current pulses (from 50 to 200 pA); two-way RM ANOVA (both factors): interaction ( F (6,78) = 1.02, p = 0.418), current injection ( F (6,78) = 39.61, p
    Figure Legend Snippet: TTA-P2 reduced tonic and rebound burst firing in CeM neurons. A , Original traces from a representative neuron in the CeM before application of TTA-P2 (left panel, orange trace), after application of TTA-P2 (middle panel, violet trace) and after wash (right panel, orange trace). Resting membrane potentials (shown in the lower left corner of each panel) show active membrane responses to a depolarizing (100 pA) current injection. B , TTA-P2 reduced tonic AP firing frequency across all current pulses (from 50 to 200 pA); two-way RM ANOVA (both factors): interaction ( F (6,78) = 1.02, p = 0.418), current injection ( F (6,78) = 39.61, p

    Techniques Used: Injection

    Mechanisms of T-current inhibition by TTA-P2. A , Traces of inward calcium current in a representative CeM neuron in control conditions recorded with TMA ATP-free internal solution using a double-pulse protocol with 3.6-s-long prepulses to variable voltages; left panel, from –120 to –95 mV in 5-mV increments (control); right panel, traces from the same cell using the identical voltage-protocol during an apparent steady-state inhibition of T-current in the presence of 5 μM TTA-P2. B , Average normalized current density, as calculated from the steady-state inactivation protocol. The presence of TTA-P2 (violet line and data points) decreased current density by 60–65% in comparison to the control conditions (gray line and data points). Data were analyzed with two-way RM ANOVA [interaction ( F (12,96) = 36.09, p
    Figure Legend Snippet: Mechanisms of T-current inhibition by TTA-P2. A , Traces of inward calcium current in a representative CeM neuron in control conditions recorded with TMA ATP-free internal solution using a double-pulse protocol with 3.6-s-long prepulses to variable voltages; left panel, from –120 to –95 mV in 5-mV increments (control); right panel, traces from the same cell using the identical voltage-protocol during an apparent steady-state inhibition of T-current in the presence of 5 μM TTA-P2. B , Average normalized current density, as calculated from the steady-state inactivation protocol. The presence of TTA-P2 (violet line and data points) decreased current density by 60–65% in comparison to the control conditions (gray line and data points). Data were analyzed with two-way RM ANOVA [interaction ( F (12,96) = 36.09, p

    Techniques Used: Inhibition

    TTA-P2-induced inhibition of tonic and rebound burst-firing in CeM neurons is diminished in recordings with ATP-free internal solution. A1 , Bar graph showing TTA-P2 significantly reduced tonic firing frequency of APs with an internal solution containing ATP (paired two-tailed t test; t (13) = 2.96, p = 0.011, n = 14). A2 , Bar graph showing TTA-P2 had a smaller effect on tonic firing frequency in recording conditions with an ATP-free internal solution (paired two-tailed t test; t (5) = 14, p = 0.085, n = 6). B1 , Bar graph showing TTA-P2 significantly reduced LTS amplitude of CeM neurons in conditions with ATP in the internal solution (paired two-tailed t test; t (12) = 7.14, p
    Figure Legend Snippet: TTA-P2-induced inhibition of tonic and rebound burst-firing in CeM neurons is diminished in recordings with ATP-free internal solution. A1 , Bar graph showing TTA-P2 significantly reduced tonic firing frequency of APs with an internal solution containing ATP (paired two-tailed t test; t (13) = 2.96, p = 0.011, n = 14). A2 , Bar graph showing TTA-P2 had a smaller effect on tonic firing frequency in recording conditions with an ATP-free internal solution (paired two-tailed t test; t (5) = 14, p = 0.085, n = 6). B1 , Bar graph showing TTA-P2 significantly reduced LTS amplitude of CeM neurons in conditions with ATP in the internal solution (paired two-tailed t test; t (12) = 7.14, p

    Techniques Used: Inhibition, Two Tailed Test

    20) Product Images from "Ionotropic glutamate receptor GluA4 and T‐type calcium channel Cav3.1 subunits control key aspects of synaptic transmission at the mouse L5B‐POm giant synapse"

    Article Title: Ionotropic glutamate receptor GluA4 and T‐type calcium channel Cav3.1 subunits control key aspects of synaptic transmission at the mouse L5B‐POm giant synapse

    Journal: The European Journal of Neuroscience

    doi: 10.1111/ejn.13084

    Rebound burst firing abolished in Ca V 3.1 knockdown but not in shRNA controls. (A) No rebound burst firing in the absence of T‐type channel Ca v 3.1 but preservation of tonic spikes ( n = 33). Somatic current injections of −300 pA and 400 pA applied for 300 ms. (B) T‐type blocker TTA‐P2 (3 μ m , grey dotted line, n = 5) selectively blocks burst firing. (C) Mismatch (blue, n = 23) and (D) scrambled controls (green, n = 5) exhibit burst and tonic firing.
    Figure Legend Snippet: Rebound burst firing abolished in Ca V 3.1 knockdown but not in shRNA controls. (A) No rebound burst firing in the absence of T‐type channel Ca v 3.1 but preservation of tonic spikes ( n = 33). Somatic current injections of −300 pA and 400 pA applied for 300 ms. (B) T‐type blocker TTA‐P2 (3 μ m , grey dotted line, n = 5) selectively blocks burst firing. (C) Mismatch (blue, n = 23) and (D) scrambled controls (green, n = 5) exhibit burst and tonic firing.

    Techniques Used: shRNA, Preserving

    21) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    22) Product Images from "Electrophysiological and Morphological Features of Rebound Depolarization Characterized Interneurons in Rat Superficial Spinal Dorsal Horn"

    Article Title: Electrophysiological and Morphological Features of Rebound Depolarization Characterized Interneurons in Rat Superficial Spinal Dorsal Horn

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.736879

    Differential modulation of I h and I T to RD in SG neurons. (A) The subthreshold currents recorded from SG neurons. (a) Representative traces of the subthreshold currents (I h , I T , and I A ) recorded in SG neurons. (b) The subthreshold currents were differentially distributed among SG neurons with (red) or without (black). (B) RD in SG neurons was modulated by I h . (a) Representative traces of RD elicited by a hyperpolarizing current pulse (−120 pA, 1 s) in control (black) and with 10 μM ZD7288 (red) in the absence of TTX. (b,c) . Summary of the blockage effect of ZD7288 on AP No. (b) and first spike latency of RD (c) in the absence of TTX. (C) RD in SG neurons was modulated by I T . (a) Representative traces of RD in control (black) and with 10 μM TTA-P2 (blue) in the absence of TTX. (b,c) Summary of the blockage effect of TTA-P2 on AP No. (b) and first spike latency of RD (c) in the absence of TTX. (D) Effect of ZD7288 on RD of SG neurons in the presence of TTX. (a) Representative traces of RD response in TTX (black) and in TTX along with 10 μM ZD7288 (red) in the presence of TTX. (b,c) Summary of the blockage effect of ZD7288 on AP No. (b) and first spike latency of RD (c) . (E) Effect of TTA-P2 on RD of SG neurons in the presence of TTX. (a) Representative traces of RD response in TTX (black) and in TTX along with 10 μM TTA-P2 (blue) in the presence of TTX. (b,c) Summary of the blockage effect of TTA-P2 on AP No. (b) and first spike latency of RD (c) . RD, rebound depolarization; I h , hyperpolarization-activated cation current; I T , T-type calcium current; I A , A-type current; AP, action potential; TTX, tetrodotoxin. * p
    Figure Legend Snippet: Differential modulation of I h and I T to RD in SG neurons. (A) The subthreshold currents recorded from SG neurons. (a) Representative traces of the subthreshold currents (I h , I T , and I A ) recorded in SG neurons. (b) The subthreshold currents were differentially distributed among SG neurons with (red) or without (black). (B) RD in SG neurons was modulated by I h . (a) Representative traces of RD elicited by a hyperpolarizing current pulse (−120 pA, 1 s) in control (black) and with 10 μM ZD7288 (red) in the absence of TTX. (b,c) . Summary of the blockage effect of ZD7288 on AP No. (b) and first spike latency of RD (c) in the absence of TTX. (C) RD in SG neurons was modulated by I T . (a) Representative traces of RD in control (black) and with 10 μM TTA-P2 (blue) in the absence of TTX. (b,c) Summary of the blockage effect of TTA-P2 on AP No. (b) and first spike latency of RD (c) in the absence of TTX. (D) Effect of ZD7288 on RD of SG neurons in the presence of TTX. (a) Representative traces of RD response in TTX (black) and in TTX along with 10 μM ZD7288 (red) in the presence of TTX. (b,c) Summary of the blockage effect of ZD7288 on AP No. (b) and first spike latency of RD (c) . (E) Effect of TTA-P2 on RD of SG neurons in the presence of TTX. (a) Representative traces of RD response in TTX (black) and in TTX along with 10 μM TTA-P2 (blue) in the presence of TTX. (b,c) Summary of the blockage effect of TTA-P2 on AP No. (b) and first spike latency of RD (c) . RD, rebound depolarization; I h , hyperpolarization-activated cation current; I T , T-type calcium current; I A , A-type current; AP, action potential; TTX, tetrodotoxin. * p

    Techniques Used:

    23) Product Images from "Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro"

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2017.04.002

    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Figure Legend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Techniques Used: Incubation, Blocking Assay, Injection

    24) Product Images from "Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro"

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2017.04.002

    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Figure Legend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Techniques Used: Incubation, Blocking Assay, Injection

    25) Product Images from "Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro"

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2017.04.002

    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Figure Legend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Techniques Used: Incubation, Blocking Assay, Injection

    26) Product Images from "Neuroepithelial progenitors generate and propagate non-neuronal action potentials across the spinal cord"

    Article Title: Neuroepithelial progenitors generate and propagate non-neuronal action potentials across the spinal cord

    Journal: bioRxiv

    doi: 10.1101/2020.05.23.111955

    Floor-plate neuroepithelial progenitors generate recurrent action potentials during spinal SNA. a, Confocal image from an E12.5 spinal cord in open-book configuration after patch-clamp recording of a floor-plate cell. The recorded floor-plate cell (yellow asterisk) was filled with neurobiotin (NBT, red) and the spinal cord was processed for immunostaining against the transcription factor FoxA2 (green), expressed in floor-plate cells and against the transcription factor NKX2.2 (blue) expressed in neuroepithelial progenitors in the adjacent p3 domain. Note that several cells were filled by neurobiotin, indicating gap junction coupling between floor-plate cells. b, Example of current-clamp recordings obtained in a floor-plate cell in response to 10 incremental current steps (increment = 10pA) in control conditions (left traces), after application of the T-type calcium channel blocker TTA-P2 (3 μM; center traces) and subsequent addition of the sodium channel blocker TTX (1 μM; right traces). Note that action potentials triggered in floor-plate cells were only fully blocked by a combination of both channel blockers. c, Example of current-clamp recording from a floor-plate cell generating recurrent depolarization. d, Magnified view of a spontaneous depolarization revealing the presence of three distinct components: a small initial depolarization (1, from −70 to −63 mV) and a biphasic action potential (grey area magnified in insert) composed of a slow (2, from −63 to −40 mV) and fast component (3, from −40 to −5 mV). e, depolarization with a time course identical to spontaneous events could also be evoked by an electrical stimulation located 3 mm rostrally to the site of recording. Application of TTA-P2 (3 μM) fully blocked the biphasic action potential while the small initial depolarization remained unaffected. f, In situ hybridization showing the location of mRNA transcripts for the 3 known sub-types of T-type channels ( cacna1g, cacna1h, cacna1i ) in coronal sections of E12.5 mouse embryos. Note that transcripts for all 3 subunits are highly expressed in the floor-plate. g, In situ hybridization showing location of mRNA transcripts for cacna1g in an E12.5 spinal cord in open-book configuration.
    Figure Legend Snippet: Floor-plate neuroepithelial progenitors generate recurrent action potentials during spinal SNA. a, Confocal image from an E12.5 spinal cord in open-book configuration after patch-clamp recording of a floor-plate cell. The recorded floor-plate cell (yellow asterisk) was filled with neurobiotin (NBT, red) and the spinal cord was processed for immunostaining against the transcription factor FoxA2 (green), expressed in floor-plate cells and against the transcription factor NKX2.2 (blue) expressed in neuroepithelial progenitors in the adjacent p3 domain. Note that several cells were filled by neurobiotin, indicating gap junction coupling between floor-plate cells. b, Example of current-clamp recordings obtained in a floor-plate cell in response to 10 incremental current steps (increment = 10pA) in control conditions (left traces), after application of the T-type calcium channel blocker TTA-P2 (3 μM; center traces) and subsequent addition of the sodium channel blocker TTX (1 μM; right traces). Note that action potentials triggered in floor-plate cells were only fully blocked by a combination of both channel blockers. c, Example of current-clamp recording from a floor-plate cell generating recurrent depolarization. d, Magnified view of a spontaneous depolarization revealing the presence of three distinct components: a small initial depolarization (1, from −70 to −63 mV) and a biphasic action potential (grey area magnified in insert) composed of a slow (2, from −63 to −40 mV) and fast component (3, from −40 to −5 mV). e, depolarization with a time course identical to spontaneous events could also be evoked by an electrical stimulation located 3 mm rostrally to the site of recording. Application of TTA-P2 (3 μM) fully blocked the biphasic action potential while the small initial depolarization remained unaffected. f, In situ hybridization showing the location of mRNA transcripts for the 3 known sub-types of T-type channels ( cacna1g, cacna1h, cacna1i ) in coronal sections of E12.5 mouse embryos. Note that transcripts for all 3 subunits are highly expressed in the floor-plate. g, In situ hybridization showing location of mRNA transcripts for cacna1g in an E12.5 spinal cord in open-book configuration.

    Techniques Used: Patch Clamp, Immunostaining, In Situ Hybridization

    Floor-plate action potentials evoked by acetylcholine rely on both TTX-sensitive voltage-gated sodium channels and T-type voltage-gated calcium channels. a , Example of current-clamp recording showing a biphasic floor-plate action potential evoked by the application of acetylcholine (30 μM, left trace), after application of the voltage-gated sodium channel blocker TTX (1μM, middle trace) and after the subsequent addition of the T-type voltage-gated calcium channel blocker TTA-P2 (3 μM, right trace). Note that the fast component of the action potential was blocked by TTX while the slow component was only blocked after addition of TTA-P2. b , Plot quantifying the effect of TTX and TTA-P2 on the amplitude of floor-plate action potential evoked by acetylcholine.
    Figure Legend Snippet: Floor-plate action potentials evoked by acetylcholine rely on both TTX-sensitive voltage-gated sodium channels and T-type voltage-gated calcium channels. a , Example of current-clamp recording showing a biphasic floor-plate action potential evoked by the application of acetylcholine (30 μM, left trace), after application of the voltage-gated sodium channel blocker TTX (1μM, middle trace) and after the subsequent addition of the T-type voltage-gated calcium channel blocker TTA-P2 (3 μM, right trace). Note that the fast component of the action potential was blocked by TTX while the slow component was only blocked after addition of TTA-P2. b , Plot quantifying the effect of TTX and TTA-P2 on the amplitude of floor-plate action potential evoked by acetylcholine.

    Techniques Used:

    27) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    28) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    29) Product Images from "Cytosolic ATP Relieves Voltage-Dependent Inactivation of T-Type Calcium Channels and Facilitates Excitability of Neurons in the Rat Central Medial Thalamus"

    Article Title: Cytosolic ATP Relieves Voltage-Dependent Inactivation of T-Type Calcium Channels and Facilitates Excitability of Neurons in the Rat Central Medial Thalamus

    Journal: eNeuro

    doi: 10.1523/ENEURO.0016-18.2018

    Mechanisms of T-current inhibition by TTA-P2. A , Traces of inward calcium current in a representative CeM neuron in control conditions recorded with TMA ATP-free internal solution using a double-pulse protocol with 3.6-s-long prepulses to variable voltages; left panel, from –120 to –95 mV in 5-mV increments (control); right panel, traces from the same cell using the identical voltage-protocol during an apparent steady-state inhibition of T-current in the presence of 5 μM TTA-P2. B , Average normalized current density, as calculated from the steady-state inactivation protocol. The presence of TTA-P2 (violet line and data points) decreased current density by 60–65% in comparison to the control conditions (gray line and data points). Data were analyzed with two-way RM ANOVA [interaction ( F (12,96) = 36.09, p
    Figure Legend Snippet: Mechanisms of T-current inhibition by TTA-P2. A , Traces of inward calcium current in a representative CeM neuron in control conditions recorded with TMA ATP-free internal solution using a double-pulse protocol with 3.6-s-long prepulses to variable voltages; left panel, from –120 to –95 mV in 5-mV increments (control); right panel, traces from the same cell using the identical voltage-protocol during an apparent steady-state inhibition of T-current in the presence of 5 μM TTA-P2. B , Average normalized current density, as calculated from the steady-state inactivation protocol. The presence of TTA-P2 (violet line and data points) decreased current density by 60–65% in comparison to the control conditions (gray line and data points). Data were analyzed with two-way RM ANOVA [interaction ( F (12,96) = 36.09, p

    Techniques Used: Inhibition

    TTA-P2 reduced tonic and rebound burst firing in CeM neurons. A , Original traces from a representative neuron in the CeM before application of TTA-P2 (left panel, orange trace), after application of TTA-P2 (middle panel, violet trace) and after wash (right panel, orange trace). Resting membrane potentials (shown in the lower left corner of each panel) show active membrane responses to a depolarizing (100 pA) current injection. B , TTA-P2 reduced tonic AP firing frequency across all current pulses (from 50 to 200 pA); two-way RM ANOVA (both factors): interaction ( F (6,78) = 1.02, p = 0.418), current injection ( F (6,78) = 39.61, p
    Figure Legend Snippet: TTA-P2 reduced tonic and rebound burst firing in CeM neurons. A , Original traces from a representative neuron in the CeM before application of TTA-P2 (left panel, orange trace), after application of TTA-P2 (middle panel, violet trace) and after wash (right panel, orange trace). Resting membrane potentials (shown in the lower left corner of each panel) show active membrane responses to a depolarizing (100 pA) current injection. B , TTA-P2 reduced tonic AP firing frequency across all current pulses (from 50 to 200 pA); two-way RM ANOVA (both factors): interaction ( F (6,78) = 1.02, p = 0.418), current injection ( F (6,78) = 39.61, p

    Techniques Used: Injection

    TTA-P2-induced inhibition of tonic and rebound burst-firing in CeM neurons is diminished in recordings with ATP-free internal solution. A1 , Bar graph showing TTA-P2 significantly reduced tonic firing frequency of APs with an internal solution containing ATP (paired two-tailed t test; t (13) = 2.96, p = 0.011, n = 14). A2 , Bar graph showing TTA-P2 had a smaller effect on tonic firing frequency in recording conditions with an ATP-free internal solution (paired two-tailed t test; t (5) = 14, p = 0.085, n = 6). B1 , Bar graph showing TTA-P2 significantly reduced LTS amplitude of CeM neurons in conditions with ATP in the internal solution (paired two-tailed t test; t (12) = 7.14, p
    Figure Legend Snippet: TTA-P2-induced inhibition of tonic and rebound burst-firing in CeM neurons is diminished in recordings with ATP-free internal solution. A1 , Bar graph showing TTA-P2 significantly reduced tonic firing frequency of APs with an internal solution containing ATP (paired two-tailed t test; t (13) = 2.96, p = 0.011, n = 14). A2 , Bar graph showing TTA-P2 had a smaller effect on tonic firing frequency in recording conditions with an ATP-free internal solution (paired two-tailed t test; t (5) = 14, p = 0.085, n = 6). B1 , Bar graph showing TTA-P2 significantly reduced LTS amplitude of CeM neurons in conditions with ATP in the internal solution (paired two-tailed t test; t (12) = 7.14, p

    Techniques Used: Inhibition, Two Tailed Test

    30) Product Images from "Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels"

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0117-17.2017

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application
    Figure Legend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Techniques Used:

    31) Product Images from "Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro"

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2017.04.002

    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Figure Legend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Techniques Used: Incubation, Blocking Assay, Injection

    32) Product Images from "Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels) Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels"

    Article Title: Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels) Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.14149

    Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis through a T‐type VGCC sensitive pathway. (A) Representative images showing immunoreactivities to dendritic and synaptic markers in DRG/spinal cord neuron co‐cultures in the presence or absence of TSP4 (20 nM) and with or without indicated VGCC blockers for 4 days. Scale bar = 10 μm. (B) Summarized data showing that only T‐type VGCC blocker TTA‐P2, but not any other VGCC blockers tested, could block Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis. Means ± SEM from 20 neurons per group that were randomly selected from four wells of multiple culture plates of independent experiments. * P
    Figure Legend Snippet: Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis through a T‐type VGCC sensitive pathway. (A) Representative images showing immunoreactivities to dendritic and synaptic markers in DRG/spinal cord neuron co‐cultures in the presence or absence of TSP4 (20 nM) and with or without indicated VGCC blockers for 4 days. Scale bar = 10 μm. (B) Summarized data showing that only T‐type VGCC blocker TTA‐P2, but not any other VGCC blockers tested, could block Ca v α 2 δ 1 /TSP4‐mediated excitatory synaptogenesis. Means ± SEM from 20 neurons per group that were randomly selected from four wells of multiple culture plates of independent experiments. * P

    Techniques Used: Blocking Assay

    33) Product Images from "Accumulation of Cav3.2 T-type Calcium Channels in the Uninjured Sural Nerve Contributes to Neuropathic Pain in Rats with Spared Nerve Injury"

    Article Title: Accumulation of Cav3.2 T-type Calcium Channels in the Uninjured Sural Nerve Contributes to Neuropathic Pain in Rats with Spared Nerve Injury

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2018.00024

    Perineural application of mibefradil or TTA-P2 decreased mechanical allodynia at day 14 after SNI. (A,B) Ipsilateral perineural perfusion of mibefradil (1.0 mM, 100 μl) or TTA-P2 (0.5 mM, 100 μl) partially reversed mechanical allodynia in a time-dependent manner. ** p
    Figure Legend Snippet: Perineural application of mibefradil or TTA-P2 decreased mechanical allodynia at day 14 after SNI. (A,B) Ipsilateral perineural perfusion of mibefradil (1.0 mM, 100 μl) or TTA-P2 (0.5 mM, 100 μl) partially reversed mechanical allodynia in a time-dependent manner. ** p

    Techniques Used:

    34) Product Images from "Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord"

    Article Title: Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00370

    Effect of T-type calcium channel blockers on the intrinsic membrane properties of SG neurons. (A) Representative T-type current traces in response to voltage-clamp protocol shown below traces in the treatment of control (black) and TTA-P2 (red). (B) Population data showing the peak amplitude of T-type currents in the absence (black) and presence of TTA-P2 (red). (C) Examples of depolarizing and hyperpolarizing traces in response to current-clamp protocols shown below traces before (black) and after (red) the treatment of TTA-P2. (D) Population data showing the rebound depolarization-evoked spike frequency plotted as a function of test potentials in the absence (black) and presence of TTA-P2 (red). (E) Population data showing the AP spike frequency plotted as a function of elicited currents in the absence (black) and presence of TTA-P2 (red). (F) Bar plots showing the various intrinsic membrane properties of SG neurons in the treatment of control (black) and TTA-P2 (red). V membrane : membrane potential measured at I hold = 0. * P
    Figure Legend Snippet: Effect of T-type calcium channel blockers on the intrinsic membrane properties of SG neurons. (A) Representative T-type current traces in response to voltage-clamp protocol shown below traces in the treatment of control (black) and TTA-P2 (red). (B) Population data showing the peak amplitude of T-type currents in the absence (black) and presence of TTA-P2 (red). (C) Examples of depolarizing and hyperpolarizing traces in response to current-clamp protocols shown below traces before (black) and after (red) the treatment of TTA-P2. (D) Population data showing the rebound depolarization-evoked spike frequency plotted as a function of test potentials in the absence (black) and presence of TTA-P2 (red). (E) Population data showing the AP spike frequency plotted as a function of elicited currents in the absence (black) and presence of TTA-P2 (red). (F) Bar plots showing the various intrinsic membrane properties of SG neurons in the treatment of control (black) and TTA-P2 (red). V membrane : membrane potential measured at I hold = 0. * P

    Techniques Used:

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    Alomone Labs tta p2
    The selective T-type calcium channel inhibitor, <t>TTA-P2,</t> blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
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    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Journal: Neuroscience

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    doi: 10.1016/j.neuroscience.2017.04.002

    Figure Lengend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Article Snippet: TTA-P2 is a potent and selective blocker of T-type calcium channels in rat sensory neurons and a novel antinociceptive agent.

    Techniques: Incubation, Blocking Assay, Injection

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Journal: The Journal of Neuroscience

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    doi: 10.1523/JNEUROSCI.0117-17.2017

    Figure Lengend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Article Snippet: Comparing TTA-P2 application to time-matched no-drug control experiments, we found that TTA-P2 significantly increased the duration of the rebound delay 6–8 min after application (control, 103 ± 2.3% n = 6 cells from 4 mice; TTA-P2, 138 ± 13.6%, n = 7 cells from 4 mice; Mann–Whitney U test, p = 0.0023), and substantially reduced the rebound dendritic Ca2+ signal (control, 86 ± 8.9%; TTA-P2, 49 ± 7.9%; Mann–Whitney U test, p = 0.014; A–C ).

    Techniques:

    Perineural application of mibefradil or TTA-P2 decreased mechanical allodynia at day 14 after SNI. (A,B) Ipsilateral perineural perfusion of mibefradil (1.0 mM, 100 μl) or TTA-P2 (0.5 mM, 100 μl) partially reversed mechanical allodynia in a time-dependent manner. ** p

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Accumulation of Cav3.2 T-type Calcium Channels in the Uninjured Sural Nerve Contributes to Neuropathic Pain in Rats with Spared Nerve Injury

    doi: 10.3389/fnmol.2018.00024

    Figure Lengend Snippet: Perineural application of mibefradil or TTA-P2 decreased mechanical allodynia at day 14 after SNI. (A,B) Ipsilateral perineural perfusion of mibefradil (1.0 mM, 100 μl) or TTA-P2 (0.5 mM, 100 μl) partially reversed mechanical allodynia in a time-dependent manner. ** p

    Article Snippet: TTA-P2 (a novel, selective T-type calcium channel blocker; Alomone Labs, Jerusalem, Israel) was dissolved in dimethyl sulfoxide (DMSO) to a 10 mM stock solution, stored at −20°C, and diluted to desired concentrations just before use.

    Techniques: