m nimodipine  (Alomone Labs)


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    Structured Review

    Alomone Labs m nimodipine
    Effects of Ca 2+ channel inhibitors on peak and trough Ca 2+ concentration. ( A and B ) Time course of the change in Ca 2+ concentration (ΔCa 2+ = Ca 2+ – average Ca 2+ from 2-min baseline) before and after the application of vehicle control (Veh) or Ca 2+ channel inhibitors at the peak ( A ) and trough ( B ). Data are mean ± SEM. ( C and D ) Plots of median, 25th and 75th percentile ( boxes ), and minimal and maximal ( whiskers ) changes in Ca 2+ concentration for individual slices quantified from 9 to 10 min after drugs were applied at the peak ( C ) and trough ( D ). Inhibition of L-type Ca 2+ channels with <t>nimodipine</t> (Nim, 10 μ M) or inhibition of N/P/Q/R/T-type Ca 2+ channels with VGC (a mixture of 3 μ M ConoGVIA, 200 nM AgaIVA, 30 μ M nickel, and 1 μ M TTA-P2) did not significantly affect peak or trough Ca 2+ levels compared to Veh. Inhibition of ryanodine receptors with dantrolene (Dan, 10 μ M), inhibition of SERCA-ATPase with cyclopiazonic acid (CPA, 10 μ M) and combined inhibition of voltage-gated Ca 2+ channels and ryanodine receptors with a cocktail containing Dan, Nim, and VGC (cocktail X) significantly decreased Ca 2+ at peak and trough. * p
    M Nimodipine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Comparative Ca2+ channel contributions to intracellular Ca2+ levels in the circadian clock"

    Article Title: Comparative Ca2+ channel contributions to intracellular Ca2+ levels in the circadian clock

    Journal: Biophysical reports

    doi: 10.1016/j.bpr.2021.100005

    Effects of Ca 2+ channel inhibitors on peak and trough Ca 2+ concentration. ( A and B ) Time course of the change in Ca 2+ concentration (ΔCa 2+ = Ca 2+ – average Ca 2+ from 2-min baseline) before and after the application of vehicle control (Veh) or Ca 2+ channel inhibitors at the peak ( A ) and trough ( B ). Data are mean ± SEM. ( C and D ) Plots of median, 25th and 75th percentile ( boxes ), and minimal and maximal ( whiskers ) changes in Ca 2+ concentration for individual slices quantified from 9 to 10 min after drugs were applied at the peak ( C ) and trough ( D ). Inhibition of L-type Ca 2+ channels with nimodipine (Nim, 10 μ M) or inhibition of N/P/Q/R/T-type Ca 2+ channels with VGC (a mixture of 3 μ M ConoGVIA, 200 nM AgaIVA, 30 μ M nickel, and 1 μ M TTA-P2) did not significantly affect peak or trough Ca 2+ levels compared to Veh. Inhibition of ryanodine receptors with dantrolene (Dan, 10 μ M), inhibition of SERCA-ATPase with cyclopiazonic acid (CPA, 10 μ M) and combined inhibition of voltage-gated Ca 2+ channels and ryanodine receptors with a cocktail containing Dan, Nim, and VGC (cocktail X) significantly decreased Ca 2+ at peak and trough. * p
    Figure Legend Snippet: Effects of Ca 2+ channel inhibitors on peak and trough Ca 2+ concentration. ( A and B ) Time course of the change in Ca 2+ concentration (ΔCa 2+ = Ca 2+ – average Ca 2+ from 2-min baseline) before and after the application of vehicle control (Veh) or Ca 2+ channel inhibitors at the peak ( A ) and trough ( B ). Data are mean ± SEM. ( C and D ) Plots of median, 25th and 75th percentile ( boxes ), and minimal and maximal ( whiskers ) changes in Ca 2+ concentration for individual slices quantified from 9 to 10 min after drugs were applied at the peak ( C ) and trough ( D ). Inhibition of L-type Ca 2+ channels with nimodipine (Nim, 10 μ M) or inhibition of N/P/Q/R/T-type Ca 2+ channels with VGC (a mixture of 3 μ M ConoGVIA, 200 nM AgaIVA, 30 μ M nickel, and 1 μ M TTA-P2) did not significantly affect peak or trough Ca 2+ levels compared to Veh. Inhibition of ryanodine receptors with dantrolene (Dan, 10 μ M), inhibition of SERCA-ATPase with cyclopiazonic acid (CPA, 10 μ M) and combined inhibition of voltage-gated Ca 2+ channels and ryanodine receptors with a cocktail containing Dan, Nim, and VGC (cocktail X) significantly decreased Ca 2+ at peak and trough. * p

    Techniques Used: Concentration Assay, Inhibition

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    Alomone Labs nimodipine
    CNQX and <t>nimodipine</t> significantly attenuate CX614-induced increases in BDNF mRNA content. Scatter graphs show BDNF cRNA-labeling densities (μCi/gm) in the stratum granulosum ( A, C ), the CA3 stratum pyramidale ( B ), and the entorhinal cortex layers
    Nimodipine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Alomone Labs qx 314
    Somatic voltage-clamp recordings from a single mitral cell, depicting responses to orthodromic stimulation of the olfactory nerve ( A ), antidromic stimulation below the mitral cell layer ( B ), and spontaneous LLDs ( E ). Antidromic and orthodromic stimulation evoke highly reproducible and nearly identical LLDs (compare A , B ). This is consistent with LLDs being generated by interactions among M/T cells. In this cell, recorded without <t>QX-314,</t> antidromically evoked LLDs are preceded by an antidromic spike ( B ). To quantify the variance of the evoked LLDs, we plotted the SDs ( SDev ) of the averaged traces ( C , D ). The largest variance occurs during the late component of the rising phase of the LLDs (delineated by the vertical dashed lines ). This is also consistent with the hypothesis that LLDs are generated by multiple interactions among M/T cells. The plot in C is shown at higher magnification in the inset . Filled circles correspond to the time points used in the text to represent the group variance data (at 20 msec after stimulus, the peak of the SD, and the peak of the LLD). F , Averaged spontaneous LLDs and their variance obtained from the traces depicted in E . Individual traces were aligned relative to the onset of their fastest component ( F, first vertical dashed line ); as in the evoked LLDs, variability is largest before the peak. G , Autocorrelogram of spontaneous LLDs ( thick line ) and peristimulus histogram ( bars ) of evoked LLDs (excluding the initial LLD) shows the similar refractory period for both spontaneous and evoked responses.
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    Alomone Labs trk inhibitor k252a
    Somatic voltage-clamp recordings from a single mitral cell, depicting responses to orthodromic stimulation of the olfactory nerve ( A ), antidromic stimulation below the mitral cell layer ( B ), and spontaneous LLDs ( E ). Antidromic and orthodromic stimulation evoke highly reproducible and nearly identical LLDs (compare A , B ). This is consistent with LLDs being generated by interactions among M/T cells. In this cell, recorded without <t>QX-314,</t> antidromically evoked LLDs are preceded by an antidromic spike ( B ). To quantify the variance of the evoked LLDs, we plotted the SDs ( SDev ) of the averaged traces ( C , D ). The largest variance occurs during the late component of the rising phase of the LLDs (delineated by the vertical dashed lines ). This is also consistent with the hypothesis that LLDs are generated by multiple interactions among M/T cells. The plot in C is shown at higher magnification in the inset . Filled circles correspond to the time points used in the text to represent the group variance data (at 20 msec after stimulus, the peak of the SD, and the peak of the LLD). F , Averaged spontaneous LLDs and their variance obtained from the traces depicted in E . Individual traces were aligned relative to the onset of their fastest component ( F, first vertical dashed line ); as in the evoked LLDs, variability is largest before the peak. G , Autocorrelogram of spontaneous LLDs ( thick line ) and peristimulus histogram ( bars ) of evoked LLDs (excluding the initial LLD) shows the similar refractory period for both spontaneous and evoked responses.
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    CNQX and nimodipine significantly attenuate CX614-induced increases in BDNF mRNA content. Scatter graphs show BDNF cRNA-labeling densities (μCi/gm) in the stratum granulosum ( A, C ), the CA3 stratum pyramidale ( B ), and the entorhinal cortex layers

    Journal: The Journal of Neuroscience

    Article Title: Positive Modulation of AMPA Receptors Increases Neurotrophin Expression by Hippocampal and Cortical Neurons

    doi: 10.1523/JNEUROSCI.20-01-00008.2000

    Figure Lengend Snippet: CNQX and nimodipine significantly attenuate CX614-induced increases in BDNF mRNA content. Scatter graphs show BDNF cRNA-labeling densities (μCi/gm) in the stratum granulosum ( A, C ), the CA3 stratum pyramidale ( B ), and the entorhinal cortex layers

    Article Snippet: For experiments using CNQX (20 μ m; Tocris Cookson, Ballwin, MO), APV (100 μ m; Tocris Cookson), nimodipine (20 μ m; Alomone Labs, Jerusalem, Israel), or CoCl2 (5 m m; Sigma), cultured slices were first pretreated (1 hr for CNQX and APV, 30 min for nimodipine, and 10 min for CoCl2 ) with either the blocker or vehicle in media and then treated for 3 hr with either blocker alone, blocker + 50 μ m CX614, 50 μ m CX614 alone, or vehicle.

    Techniques: Labeling

    Effects of Ca 2+ channel inhibitors on peak and trough Ca 2+ concentration. ( A and B ) Time course of the change in Ca 2+ concentration (ΔCa 2+ = Ca 2+ – average Ca 2+ from 2-min baseline) before and after the application of vehicle control (Veh) or Ca 2+ channel inhibitors at the peak ( A ) and trough ( B ). Data are mean ± SEM. ( C and D ) Plots of median, 25th and 75th percentile ( boxes ), and minimal and maximal ( whiskers ) changes in Ca 2+ concentration for individual slices quantified from 9 to 10 min after drugs were applied at the peak ( C ) and trough ( D ). Inhibition of L-type Ca 2+ channels with nimodipine (Nim, 10 μ M) or inhibition of N/P/Q/R/T-type Ca 2+ channels with VGC (a mixture of 3 μ M ConoGVIA, 200 nM AgaIVA, 30 μ M nickel, and 1 μ M TTA-P2) did not significantly affect peak or trough Ca 2+ levels compared to Veh. Inhibition of ryanodine receptors with dantrolene (Dan, 10 μ M), inhibition of SERCA-ATPase with cyclopiazonic acid (CPA, 10 μ M) and combined inhibition of voltage-gated Ca 2+ channels and ryanodine receptors with a cocktail containing Dan, Nim, and VGC (cocktail X) significantly decreased Ca 2+ at peak and trough. * p

    Journal: Biophysical reports

    Article Title: Comparative Ca2+ channel contributions to intracellular Ca2+ levels in the circadian clock

    doi: 10.1016/j.bpr.2021.100005

    Figure Lengend Snippet: Effects of Ca 2+ channel inhibitors on peak and trough Ca 2+ concentration. ( A and B ) Time course of the change in Ca 2+ concentration (ΔCa 2+ = Ca 2+ – average Ca 2+ from 2-min baseline) before and after the application of vehicle control (Veh) or Ca 2+ channel inhibitors at the peak ( A ) and trough ( B ). Data are mean ± SEM. ( C and D ) Plots of median, 25th and 75th percentile ( boxes ), and minimal and maximal ( whiskers ) changes in Ca 2+ concentration for individual slices quantified from 9 to 10 min after drugs were applied at the peak ( C ) and trough ( D ). Inhibition of L-type Ca 2+ channels with nimodipine (Nim, 10 μ M) or inhibition of N/P/Q/R/T-type Ca 2+ channels with VGC (a mixture of 3 μ M ConoGVIA, 200 nM AgaIVA, 30 μ M nickel, and 1 μ M TTA-P2) did not significantly affect peak or trough Ca 2+ levels compared to Veh. Inhibition of ryanodine receptors with dantrolene (Dan, 10 μ M), inhibition of SERCA-ATPase with cyclopiazonic acid (CPA, 10 μ M) and combined inhibition of voltage-gated Ca 2+ channels and ryanodine receptors with a cocktail containing Dan, Nim, and VGC (cocktail X) significantly decreased Ca 2+ at peak and trough. * p

    Article Snippet: Pharmacological reagents were used at final concentrations of 10 μ M nimodipine (Nim; N150; Alomone Labs, Jerusalem, Israel), 10 μ M dantrolene (Dan; D9175; Sigma-Aldrich), 30 μ M CPA (C-750; Alomone Labs), 3 μ M ω -conotoxin GVIA (ConoGVIA; C-300; Alomone Labs), 200 nM ω -agatoxin IVA (AgaIVA; STA-500; Alomone Labs), 30 μ M NiCl2 (Ni2+ ; 22387; Sigma-Aldrich), 10 μ M ionomycin (407951; Sigma-Aldrich), 10 μ M rotenone (R8875; Sigma-Aldrich), and 50 mM KCl (P9333; Sigma-Aldrich).

    Techniques: Concentration Assay, Inhibition

    Somatic voltage-clamp recordings from a single mitral cell, depicting responses to orthodromic stimulation of the olfactory nerve ( A ), antidromic stimulation below the mitral cell layer ( B ), and spontaneous LLDs ( E ). Antidromic and orthodromic stimulation evoke highly reproducible and nearly identical LLDs (compare A , B ). This is consistent with LLDs being generated by interactions among M/T cells. In this cell, recorded without QX-314, antidromically evoked LLDs are preceded by an antidromic spike ( B ). To quantify the variance of the evoked LLDs, we plotted the SDs ( SDev ) of the averaged traces ( C , D ). The largest variance occurs during the late component of the rising phase of the LLDs (delineated by the vertical dashed lines ). This is also consistent with the hypothesis that LLDs are generated by multiple interactions among M/T cells. The plot in C is shown at higher magnification in the inset . Filled circles correspond to the time points used in the text to represent the group variance data (at 20 msec after stimulus, the peak of the SD, and the peak of the LLD). F , Averaged spontaneous LLDs and their variance obtained from the traces depicted in E . Individual traces were aligned relative to the onset of their fastest component ( F, first vertical dashed line ); as in the evoked LLDs, variability is largest before the peak. G , Autocorrelogram of spontaneous LLDs ( thick line ) and peristimulus histogram ( bars ) of evoked LLDs (excluding the initial LLD) shows the similar refractory period for both spontaneous and evoked responses.

    Journal: The Journal of Neuroscience

    Article Title: Long-Lasting Depolarizations in Mitral Cells of the Rat Olfactory Bulb

    doi: 10.1523/JNEUROSCI.20-05-02011.2000

    Figure Lengend Snippet: Somatic voltage-clamp recordings from a single mitral cell, depicting responses to orthodromic stimulation of the olfactory nerve ( A ), antidromic stimulation below the mitral cell layer ( B ), and spontaneous LLDs ( E ). Antidromic and orthodromic stimulation evoke highly reproducible and nearly identical LLDs (compare A , B ). This is consistent with LLDs being generated by interactions among M/T cells. In this cell, recorded without QX-314, antidromically evoked LLDs are preceded by an antidromic spike ( B ). To quantify the variance of the evoked LLDs, we plotted the SDs ( SDev ) of the averaged traces ( C , D ). The largest variance occurs during the late component of the rising phase of the LLDs (delineated by the vertical dashed lines ). This is also consistent with the hypothesis that LLDs are generated by multiple interactions among M/T cells. The plot in C is shown at higher magnification in the inset . Filled circles correspond to the time points used in the text to represent the group variance data (at 20 msec after stimulus, the peak of the SD, and the peak of the LLD). F , Averaged spontaneous LLDs and their variance obtained from the traces depicted in E . Individual traces were aligned relative to the onset of their fastest component ( F, first vertical dashed line ); as in the evoked LLDs, variability is largest before the peak. G , Autocorrelogram of spontaneous LLDs ( thick line ) and peristimulus histogram ( bars ) of evoked LLDs (excluding the initial LLD) shows the similar refractory period for both spontaneous and evoked responses.

    Article Snippet: Unless otherwise indicated, all voltage-clamp recordings were performed with QX-314 (10 m m ) in the electrode to suppress Na+ spikes.

    Techniques: Generated