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pkcε translocation inhibitor peptide εv1 2 eavslkpt  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology pkcε translocation inhibitor peptide εv1 2 eavslkpt
    Pkcε Translocation Inhibitor Peptide εv1 2 Eavslkpt, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pkcε translocation inhibitor peptide εv1 2 eavslkpt/product/Santa Cruz Biotechnology
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    pkcε translocation inhibitor peptide εv1 2 eavslkpt  (Santa Cruz Biotechnology)
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    Characteristics of the GR73632-evoked SP release from cultured adult rat DRG neurons . Some cells were left untreated as a control, all other cells were treated with GR73632 alone or together with three MAP kinases <t>cascades</t> <t>inhibitors</t> (10 μM U0126, 15 μM SB203580 and 30 μM SP600125), PLC inhibitor (10 μM U73122) or with COX inhibitors (1 μM NS-398 and 1 μM indomethacin), PKC inhibitors (1 μM Gö6976, 1 μM bisindolymaleimide, 200 μM <t>PKCε</t> translocation inhibitor peptide) or with PKA inhibitor (10 μM H89) in DMEM (serum free) for 60 min. The data are expressed as the means ± S.E.M. (bars) from 3–5 (A), 6 (B) or 4 (C), 4 (D) separate experiments. *, ** and *** denote p < 0.05, 0.01 and 0.001, respectively.
    Pkcε Translocation Inhibitor Peptide εv1 2 Eavslkpt, supplied by Santa Cruz Biotechnology, 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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    Image Search Results


    PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Article Snippet: #539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.001), n = 21 , 12.62 ± 8.427.

    Techniques: Produced, Derivative Assay, Inhibition, Translocation Assay, Transferring

    Summary of inhibitors and results ( n = cell numbers).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Summary of inhibitors and results ( n = cell numbers).

    Article Snippet: #539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.001), n = 21 , 12.62 ± 8.427.

    Techniques: Translocation Assay, Negative Control

    Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Article Snippet: #539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.001), n = 21 , 12.62 ± 8.427.

    Techniques: Transferring

    Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Article Snippet: #539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.001), n = 21 , 12.62 ± 8.427.

    Techniques: Translocation Assay, Membrane, Injection, Control

    T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Article Snippet: #539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.001), n = 21 , 12.62 ± 8.427.

    Techniques: Membrane, Control

    PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Produced, Derivative Assay, Inhibition, Translocation Assay, Transferring

    Summary of inhibitors and results ( n = cell numbers).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Summary of inhibitors and results ( n = cell numbers).

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Translocation Assay, Negative Control

    Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Transferring

    Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Translocation Assay, Membrane, Injection, Control

    T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Membrane, Control

    PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Article Snippet: As a control, we used a PKCε translocation inhibitor inactive peptide (negative control, sequence of #539542: H-Leu-Ser-Glu-Thr-Lys-Pro-Ala-Val-OH, 5 μM, Calbiochem, Burlington, MA) as well as a scrambled peptide with an identical amino acid composition to that of a PKCε translocation inhibitor peptide (#539522) delivered in the internal solution.

    Techniques: Produced, Derivative Assay, Inhibition, Translocation Assay, Transferring

    Summary of inhibitors and results ( n = cell numbers).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Summary of inhibitors and results ( n = cell numbers).

    Article Snippet: As a control, we used a PKCε translocation inhibitor inactive peptide (negative control, sequence of #539542: H-Leu-Ser-Glu-Thr-Lys-Pro-Ala-Val-OH, 5 μM, Calbiochem, Burlington, MA) as well as a scrambled peptide with an identical amino acid composition to that of a PKCε translocation inhibitor peptide (#539522) delivered in the internal solution.

    Techniques: Translocation Assay, Negative Control

    Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Article Snippet: As a control, we used a PKCε translocation inhibitor inactive peptide (negative control, sequence of #539542: H-Leu-Ser-Glu-Thr-Lys-Pro-Ala-Val-OH, 5 μM, Calbiochem, Burlington, MA) as well as a scrambled peptide with an identical amino acid composition to that of a PKCε translocation inhibitor peptide (#539522) delivered in the internal solution.

    Techniques: Transferring

    Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Article Snippet: As a control, we used a PKCε translocation inhibitor inactive peptide (negative control, sequence of #539542: H-Leu-Ser-Glu-Thr-Lys-Pro-Ala-Val-OH, 5 μM, Calbiochem, Burlington, MA) as well as a scrambled peptide with an identical amino acid composition to that of a PKCε translocation inhibitor peptide (#539522) delivered in the internal solution.

    Techniques: Translocation Assay, Membrane, Injection, Control

    T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Article Snippet: As a control, we used a PKCε translocation inhibitor inactive peptide (negative control, sequence of #539542: H-Leu-Ser-Glu-Thr-Lys-Pro-Ala-Val-OH, 5 μM, Calbiochem, Burlington, MA) as well as a scrambled peptide with an identical amino acid composition to that of a PKCε translocation inhibitor peptide (#539522) delivered in the internal solution.

    Techniques: Membrane, Control

    PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Article Snippet: # 539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.026), n = 25 (−100 pA) , 1.971 ± 1.783.

    Techniques: Produced, Derivative Assay, Inhibition, Translocation Assay, Transferring

    Summary of inhibitors and results ( n = cell numbers).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Summary of inhibitors and results ( n = cell numbers).

    Article Snippet: # 539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.026), n = 25 (−100 pA) , 1.971 ± 1.783.

    Techniques: Translocation Assay, Negative Control

    Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Article Snippet: # 539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.026), n = 25 (−100 pA) , 1.971 ± 1.783.

    Techniques: Transferring

    Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Article Snippet: # 539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.026), n = 25 (−100 pA) , 1.971 ± 1.783.

    Techniques: Translocation Assay, Membrane, Injection, Control

    T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Article Snippet: # 539522 (Calbiochem) , PKCε translocation inhibitor , WD vs WD + PKCε (−) , Reduction (p = 0.026), n = 25 (−100 pA) , 1.971 ± 1.783.

    Techniques: Membrane, Control

    Characteristics of the GR73632-evoked SP release from cultured adult rat DRG neurons . Some cells were left untreated as a control, all other cells were treated with GR73632 alone or together with three MAP kinases cascades inhibitors (10 μM U0126, 15 μM SB203580 and 30 μM SP600125), PLC inhibitor (10 μM U73122) or with COX inhibitors (1 μM NS-398 and 1 μM indomethacin), PKC inhibitors (1 μM Gö6976, 1 μM bisindolymaleimide, 200 μM PKCε translocation inhibitor peptide) or with PKA inhibitor (10 μM H89) in DMEM (serum free) for 60 min. The data are expressed as the means ± S.E.M. (bars) from 3–5 (A), 6 (B) or 4 (C), 4 (D) separate experiments. *, ** and *** denote p < 0.05, 0.01 and 0.001, respectively.

    Journal: Molecular Pain

    Article Title: Activation of the neurokinin-1 receptor by substance P triggers the release of substance P from cultured adult rat dorsal root ganglion neurons

    doi: 10.1186/1744-8069-3-42

    Figure Lengend Snippet: Characteristics of the GR73632-evoked SP release from cultured adult rat DRG neurons . Some cells were left untreated as a control, all other cells were treated with GR73632 alone or together with three MAP kinases cascades inhibitors (10 μM U0126, 15 μM SB203580 and 30 μM SP600125), PLC inhibitor (10 μM U73122) or with COX inhibitors (1 μM NS-398 and 1 μM indomethacin), PKC inhibitors (1 μM Gö6976, 1 μM bisindolymaleimide, 200 μM PKCε translocation inhibitor peptide) or with PKA inhibitor (10 μM H89) in DMEM (serum free) for 60 min. The data are expressed as the means ± S.E.M. (bars) from 3–5 (A), 6 (B) or 4 (C), 4 (D) separate experiments. *, ** and *** denote p < 0.05, 0.01 and 0.001, respectively.

    Article Snippet: Except for some cultured cells treated by peptidase inhibitors containing 1 μM phosphoramidon (Sigma), 4 μg/ml bacitracin (Sigma) and 1 μM captopril (Sigma) alone (as a control), other cultured cells were exposed to SP (Peptide Institute, Osaka, Japan) or to GR73632 (Sigma), either alone or together with various inhibitors such as Gö6976 (Calbiochem, Darmstadt, Germany), PKCε translocation inhibitor peptide (Calbiochem) and bisindolylmaleimide I (Calbiochem), indomethacin (Sigma) and SB222200 (Sigma), GR94800 (Sigma) and U73122 (Sigma), SP600125 (Sigma) and H89 (Seikagaku, Tokyo, Japan) in 1 ml serum-free DMEM (Nissui, Tokyo, Japan) containing peptidase inhibitors for a designated period of time at 37°C in a water-saturated atmosphere with 5% CO 2 .

    Techniques: Cell Culture, Translocation Assay

    Effects of SP and GR73632 on COX-2 protein expression in cultured adult rat DRG neurons . (A) The time-dependence of COX-2 expression in cultured DRG neurons exposed to SP. (B) The protein levels of COX-2 in DRG neurons treated with GR73632, either alone or together with 1 μM CP-96,345, three MAP kinases cascades inhibitors (10 μM U0126, 15 μM SB203580 and 30 μM SP600125) or with 1 μM NS-398, PKC inhibitors (1 μM Gö6976, 1 μM bisindolymaleimide, 200 μM PKCε translocation inhibitor peptide) for 60 min were measured by Western blot analysis. All data have been normalized to the COX-2 expression level of control group. The data are expressed as the means ± S.E.M. (bars) from 4 (A) or 4 (B) separate experiments. *, ** and *** denote p < 0.05, 0.01 and 0.001, respectively.

    Journal: Molecular Pain

    Article Title: Activation of the neurokinin-1 receptor by substance P triggers the release of substance P from cultured adult rat dorsal root ganglion neurons

    doi: 10.1186/1744-8069-3-42

    Figure Lengend Snippet: Effects of SP and GR73632 on COX-2 protein expression in cultured adult rat DRG neurons . (A) The time-dependence of COX-2 expression in cultured DRG neurons exposed to SP. (B) The protein levels of COX-2 in DRG neurons treated with GR73632, either alone or together with 1 μM CP-96,345, three MAP kinases cascades inhibitors (10 μM U0126, 15 μM SB203580 and 30 μM SP600125) or with 1 μM NS-398, PKC inhibitors (1 μM Gö6976, 1 μM bisindolymaleimide, 200 μM PKCε translocation inhibitor peptide) for 60 min were measured by Western blot analysis. All data have been normalized to the COX-2 expression level of control group. The data are expressed as the means ± S.E.M. (bars) from 4 (A) or 4 (B) separate experiments. *, ** and *** denote p < 0.05, 0.01 and 0.001, respectively.

    Article Snippet: Except for some cultured cells treated by peptidase inhibitors containing 1 μM phosphoramidon (Sigma), 4 μg/ml bacitracin (Sigma) and 1 μM captopril (Sigma) alone (as a control), other cultured cells were exposed to SP (Peptide Institute, Osaka, Japan) or to GR73632 (Sigma), either alone or together with various inhibitors such as Gö6976 (Calbiochem, Darmstadt, Germany), PKCε translocation inhibitor peptide (Calbiochem) and bisindolylmaleimide I (Calbiochem), indomethacin (Sigma) and SB222200 (Sigma), GR94800 (Sigma) and U73122 (Sigma), SP600125 (Sigma) and H89 (Seikagaku, Tokyo, Japan) in 1 ml serum-free DMEM (Nissui, Tokyo, Japan) containing peptidase inhibitors for a designated period of time at 37°C in a water-saturated atmosphere with 5% CO 2 .

    Techniques: Expressing, Cell Culture, Translocation Assay, Western Blot