okadaic acid  (Alomone Labs)


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    Alomone Labs okadaic acid
    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM <t>okadaic</t> acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
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    Images

    1) Product Images from "Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism"

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00090

    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
    Figure Legend Snippet: Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Techniques Used: Inhibition, Activation Assay, Produced

    MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.
    Figure Legend Snippet: MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Techniques Used: Activation Assay, Inhibition, Activity Assay

    2) Product Images from "Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism"

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00090

    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
    Figure Legend Snippet: Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Techniques Used: Inhibition, Activation Assay, Produced

    MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.
    Figure Legend Snippet: MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Techniques Used: Activation Assay, Inhibition, Activity Assay

    3) Product Images from "Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism"

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00090

    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
    Figure Legend Snippet: Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Techniques Used: Inhibition, Activation Assay, Produced

    MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.
    Figure Legend Snippet: MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Techniques Used: Activation Assay, Inhibition, Activity Assay

    4) Product Images from "Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism"

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00090

    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
    Figure Legend Snippet: Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Techniques Used: Inhibition, Activation Assay, Produced

    MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.
    Figure Legend Snippet: MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Techniques Used: Activation Assay, Inhibition, Activity Assay

    5) Product Images from "Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism"

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00090

    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
    Figure Legend Snippet: Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Techniques Used: Inhibition, Activation Assay, Produced

    MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.
    Figure Legend Snippet: MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Techniques Used: Activation Assay, Inhibition, Activity Assay

    6) Product Images from "Combined kinase inhibition modulates parkin inactivation"

    Article Title: Combined kinase inhibition modulates parkin inactivation

    Journal: Human Molecular Genetics

    doi: 10.1093/hmg/ddn407

    Parkin phosphorylation by casein kinase I in cells assessed using phospho-state-specific antibodies. ( A ) Phospho-state-specific antibodies against phospho-S101 (P-Ser101) or against phospho-S378 (P-Ser378) recognize recombinant full-length parkin only upon its in vitro phosphorylation by casein kinase I (+CK1), but not if the protein is not previously subjected to phosphorylation (−CK1). ( B ) Exogenous human parkin, upon transfection in HEK293T cells (+transf.), is constitutively phosphorylated on both S101 and S378 residues. Cells were treated for 1 h with 500 n m okadaic acid before cell lysis to stabilize the phosphorylation state of parkin. ( C ) Exogenous human parkin phosphorylation on S101 and S378 decreases upon treatment of HEK293T cells with IC261 (50 µ m ), a specific inhibitor of casein kinase I.
    Figure Legend Snippet: Parkin phosphorylation by casein kinase I in cells assessed using phospho-state-specific antibodies. ( A ) Phospho-state-specific antibodies against phospho-S101 (P-Ser101) or against phospho-S378 (P-Ser378) recognize recombinant full-length parkin only upon its in vitro phosphorylation by casein kinase I (+CK1), but not if the protein is not previously subjected to phosphorylation (−CK1). ( B ) Exogenous human parkin, upon transfection in HEK293T cells (+transf.), is constitutively phosphorylated on both S101 and S378 residues. Cells were treated for 1 h with 500 n m okadaic acid before cell lysis to stabilize the phosphorylation state of parkin. ( C ) Exogenous human parkin phosphorylation on S101 and S378 decreases upon treatment of HEK293T cells with IC261 (50 µ m ), a specific inhibitor of casein kinase I.

    Techniques Used: Recombinant, In Vitro, Transfection, Lysis

    Analysis of pathogenic parkin mutants. ( A ) The percentage of transfected cells displaying parkin aggregates using wild-type or various pathogenic parkin point mutants (wt, n = 5; R256C, n = 6; R275W, n = 11; C289G, n = 10). Bars depict mean±S.E.M. ( B ) Example of an autoubiquitylation experiment using wild-type or the indicated parkin mutants, and either wild-type ubiquitin (Ub) or a lysine-less derivative (LL-Ub). ( C ) Example of in vitro phosphorylation experiments using full-length recombinant parkin (wt), or the indicated point-mutated versions, and either casein kinase I (CK1, top) or cdk5 (bottom). ( D ) Analysis of the distribution of overexpressed wild-type (wt) or the various mutant parkin proteins (total, T) in the Triton X-100-soluble (S) and insoluble pellet (P) fractions of HEK293T extracts upon blotting with a phospho-state-specific parkin antibody (P-Ser378), an anti-parkin antibody (Abcam) or an anti-actin antibody. Note that the phosphorylation status of wild-type parkin in the soluble and insoluble fractions could only be detected in the presence of okadaic acid or upon prolonged exposure of the blot (not shown).
    Figure Legend Snippet: Analysis of pathogenic parkin mutants. ( A ) The percentage of transfected cells displaying parkin aggregates using wild-type or various pathogenic parkin point mutants (wt, n = 5; R256C, n = 6; R275W, n = 11; C289G, n = 10). Bars depict mean±S.E.M. ( B ) Example of an autoubiquitylation experiment using wild-type or the indicated parkin mutants, and either wild-type ubiquitin (Ub) or a lysine-less derivative (LL-Ub). ( C ) Example of in vitro phosphorylation experiments using full-length recombinant parkin (wt), or the indicated point-mutated versions, and either casein kinase I (CK1, top) or cdk5 (bottom). ( D ) Analysis of the distribution of overexpressed wild-type (wt) or the various mutant parkin proteins (total, T) in the Triton X-100-soluble (S) and insoluble pellet (P) fractions of HEK293T extracts upon blotting with a phospho-state-specific parkin antibody (P-Ser378), an anti-parkin antibody (Abcam) or an anti-actin antibody. Note that the phosphorylation status of wild-type parkin in the soluble and insoluble fractions could only be detected in the presence of okadaic acid or upon prolonged exposure of the blot (not shown).

    Techniques Used: Transfection, In Vitro, Recombinant, Mutagenesis

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    Alomone Labs okadaic acid
    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM <t>okadaic</t> acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P
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    Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    doi: 10.3389/fncel.2014.00090

    Figure Lengend Snippet: Inhibition of the I Ca by MOR activation was reverted by 8-Br-cAMP or IBMX and mimicked by H89. (A) Time course of the I Ca amplitude under the control condition, after 1 μM DAMGO and DAMGO plus 1 mM 8-Br-cAMP application. The application of 8-Br-cAMP reverted the DAMGO inhibition 92 ± 7% ( n = 7). (B) Traces of the I Ca under the control condition, after DAMGO and after the co-application of DAMGO and 8-Br-cAMP. (C) Time course of the I Ca peak amplitude under the control condition, after the use of 1 μM H89 and after 1 μM H89 plus 1 μM DAMGO perfusion. The H89 mimicked the inhibitory effect of DAMGO; the co-application of H89 and DAMGO did not add to its inhibitory effects ( n = 9). (D) I-V relationship of calcium current showed that the phosphatase inhibition with 100 nM okadaic acid enhanced the HVA and LVA currents, shifted the peak of the IV relationship to less depolarized values, but was unable to occlude the inhibitory effect of 1 μM DAMGO. (E) Representative traces of the LVA and HVA currents in control, under perfusion with 100 nM okadaic acid and coapplication of 100 nM okadaic acid and 1 μM DAMGO. The okadaic acid enhanced the I Ca but was unable to occlude the DAMGO effect. The line dotted line represents zero current. The voltage clamp protocol is shown below the recordings. (F) Bar graph summarizing the effects produced by the various drugs used to discern the pathways involved in MOR actions upon both the LVA and HVA current components ( * means P

    Article Snippet: The use of 100 nM okadaic acid enhanced the LVA 86 ± 8% (n = 5, P = 0.02), while the co-application of DAMGO (1 μM) and okadaic acid (1 μM) decreased the current 35 ± 10% with respect to the control (n = 5, P = 0.05).

    Techniques: Inhibition, Activation Assay, Produced

    MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Activation of ?-opioid receptors inhibits calcium-currents in the vestibular afferent neurons of the rat through a cAMP dependent mechanism

    doi: 10.3389/fncel.2014.00090

    Figure Lengend Snippet: MOR activation pathway leading to I Ca inhibition in the VANs. The use of PTX showed that the I Ca inhibition by MOR activation is Gα i/o dependent. Use of paired pulses showed that the VD signaling mechanism does not significantly participate in the I Ca inhibition. The use of forskolin, 8-Br-cAMP, IBMX, H89, and okadaic acid indicate that the I Ca inhibition (LVA and HVA) by MOR activation is mediated by the cAMP pathway. Involving the Gα i/o inhibition, AC inhibition, decreased of cAMP levels, decreased of PKA activity and decreased of PKA-dependent phosphorylation of calcium channels. In the scheme, arrow-endings indicate activation and the line-endings indicate inhibition. The names and lines in red indicate the drugs used. AC, Adenylyl cyclase; GP, G Protein; PDE, Phosphodiesterase; VD, Voltage dependent signaling mechanism; VGCC, Voltage gated calcium channels; VI, Voltage independent signaling mechanism.

    Article Snippet: The use of 100 nM okadaic acid enhanced the LVA 86 ± 8% (n = 5, P = 0.02), while the co-application of DAMGO (1 μM) and okadaic acid (1 μM) decreased the current 35 ± 10% with respect to the control (n = 5, P = 0.05).

    Techniques: Activation Assay, Inhibition, Activity Assay