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  • 99
    Millipore damgo
    Histological analysis of microinfusion sites for both the <t>muscimol</t> and <t>DAMGO</t> injections. A , Nucleus accumbens placements of one representative study. The remaining slides display the placements of all subjects for each respective study. B , Dorsomedial hypothalamus, lateral hypothalamus, dorsal hippocampus ( C ), ventral tegmental area, ( D .
    Damgo, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 385 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Tocris damgo
    Selective and non-specific binding for MOR and KOR autoradiography. 1A) Selective binding of MOR using [ 3 <t>H]DAMGO</t> blocking DOR and KOR by co-incubating with <t>DPDPE</t> and U69,593, respectively 1B) Non-specific binding of MOR with [ 3 H]DAMGO and co-incubating
    Damgo, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 215 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Bachem damgo
    Relative efficacy values for <t>DAMGO,</t> <t>etorphine,</t> endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3
    Damgo, supplied by Bachem, used in various techniques. Bioz Stars score: 92/100, based on 72 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    GE Healthcare h damgo
    Relative efficacy values for <t>DAMGO,</t> <t>etorphine,</t> endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3
    H Damgo, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 99/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    damgo  (Abcam)
    94
    Abcam damgo
    Morphine inhibits IPSCs through activation of MOPs and DOPs. ( A ) Exemplar recording of the inhibition of sIPSC frequency by morphine (100 μM) in a VTA neuron, with the associated graph of cumulative probability of the inter-event intervals. ( B ) Graph of the concentration-dependent inhibition of sIPSC frequency by morphine in WT neurons (EC 50 = 2 µM (95% CIs = 0.54 and 7.2 µM), slope = 0.8, n = 5–10) and MOP+/− neurons (EC 50 = 128 µM, (95% CIs = 20 and 826 µM), slope = 0.7, n = 4–8). ( C ) Bar graph of the average inhibition by morphine (100 μM) of sIPSC frequency in WT (72 ± 5%, n = 7), MOP+/− (50 ± 9%, n = 4) and MOP−/− (11 ± 5%, n = 7) neurons. ( D ) Exemplar sIPSCs recorded from a WT neuron in the absence and presence of <t>DPDPE</t> (1 µM), with the associated graph of cumulative probabilities. ( E ) Exemplar recording from a MOP−/− neuron in the absence and presence of DPDPE, with the graph of cumulative probability. ( F ) Bar graph illustrating the average inhibition by DPDPE of sIPSC frequency in WT (37 ± 7%, n = 6), MOP−/− (34 ± 2%. n = 5) and DOP−/− neurons (7 ± 5%, n = 6). ( G ) sIPSCs recorded from a DOP−/− VTA neuron, illustrating the remaining inhibition by morphine, with the associated graph of cumulative probability. ( H ) Bar graph of inhibition of sIPSC frequency by morphine and <t>DAMGO.</t> Inhibition by morphine was reduced in DOP−/− neurons (42 ± 5%, n = 8) compared to WT neurons (64 ± 5, n = 10; unpaired t test p = 0.004; see Table 1 ). While Inhibition by DAMGO (42 ± 11%, n = 8) was not significantly different (unpaired t test p = 0.31, WT n = 7, DOP−/− n = 7) to WT (55 ± 4%, n = 7). Vertical lines represent ± SEM. One way ANOVA p
    Damgo, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Peninsula Laboratories damgo
    Morphine inhibits IPSCs through activation of MOPs and DOPs. ( A ) Exemplar recording of the inhibition of sIPSC frequency by morphine (100 μM) in a VTA neuron, with the associated graph of cumulative probability of the inter-event intervals. ( B ) Graph of the concentration-dependent inhibition of sIPSC frequency by morphine in WT neurons (EC 50 = 2 µM (95% CIs = 0.54 and 7.2 µM), slope = 0.8, n = 5–10) and MOP+/− neurons (EC 50 = 128 µM, (95% CIs = 20 and 826 µM), slope = 0.7, n = 4–8). ( C ) Bar graph of the average inhibition by morphine (100 μM) of sIPSC frequency in WT (72 ± 5%, n = 7), MOP+/− (50 ± 9%, n = 4) and MOP−/− (11 ± 5%, n = 7) neurons. ( D ) Exemplar sIPSCs recorded from a WT neuron in the absence and presence of <t>DPDPE</t> (1 µM), with the associated graph of cumulative probabilities. ( E ) Exemplar recording from a MOP−/− neuron in the absence and presence of DPDPE, with the graph of cumulative probability. ( F ) Bar graph illustrating the average inhibition by DPDPE of sIPSC frequency in WT (37 ± 7%, n = 6), MOP−/− (34 ± 2%. n = 5) and DOP−/− neurons (7 ± 5%, n = 6). ( G ) sIPSCs recorded from a DOP−/− VTA neuron, illustrating the remaining inhibition by morphine, with the associated graph of cumulative probability. ( H ) Bar graph of inhibition of sIPSC frequency by morphine and <t>DAMGO.</t> Inhibition by morphine was reduced in DOP−/− neurons (42 ± 5%, n = 8) compared to WT neurons (64 ± 5, n = 10; unpaired t test p = 0.004; see Table 1 ). While Inhibition by DAMGO (42 ± 11%, n = 8) was not significantly different (unpaired t test p = 0.31, WT n = 7, DOP−/− n = 7) to WT (55 ± 4%, n = 7). Vertical lines represent ± SEM. One way ANOVA p
    Damgo, supplied by Peninsula Laboratories, used in various techniques. Bioz Stars score: 92/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Millipore trifluoroacetate salt
    Liraglutide stimulated NO production via the cAMP/PKA/AMPK/eNOS pathway in HUVECs. NO production by HUVECs was determined by measuring levels of the stable metabolites of NO (NO 2 and NO 3 ) in the culture medium. HUVECs were stimulated with the indicated concentrations of agents (saline or liraglutide 0.1–100 nmol/L) for 2 h, following serum starvation in M199, 0.3% FBS, for 1 h. Inhibitors were added 30 min prior to stimulation at the following concentrations: GLP-1R antagonist exendin-(9–39) (Ex-9), 100 nmol/L; cAMP inhibitor SQ22536 (SQ), 100 μmol/L; cAMP-dependent protein kinase (PKA) inhibitor fragment 14–22 myristoylated <t>trifluoroacetate</t> salt (PKI[14–22]), 1 μmol/L; exchange factor directly activated by cAMP inhibitor (ESI-09), 6.4 μmol/L; calcium-calmodulin-dependent protein kinase kinase inhibitor (STO-609), 10 μmol/L; AMP-activated protein kinase (AMPK) inhibitor (dorsomorphine), 10 μmol/L; Akt inhibitor 10-(4′-[[ N -diethylamino]]butyl)-2-chlorophenoxazine (AktI X), 5 μmol/L; NOS inhibitor ( l -NAME), 1 mmol/L; a effects of liraglutide and the Ex-9 GLP-1R antagonist on endothelial NO production, 2 h after stimulation; b effects of inhibitors of downstream molecules of GLP-1R on liraglutide-stimulated NO production; n = 4–6; *p
    Trifluoroacetate Salt, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Millipore drugs damgo
    Liraglutide stimulated NO production via the cAMP/PKA/AMPK/eNOS pathway in HUVECs. NO production by HUVECs was determined by measuring levels of the stable metabolites of NO (NO 2 and NO 3 ) in the culture medium. HUVECs were stimulated with the indicated concentrations of agents (saline or liraglutide 0.1–100 nmol/L) for 2 h, following serum starvation in M199, 0.3% FBS, for 1 h. Inhibitors were added 30 min prior to stimulation at the following concentrations: GLP-1R antagonist exendin-(9–39) (Ex-9), 100 nmol/L; cAMP inhibitor SQ22536 (SQ), 100 μmol/L; cAMP-dependent protein kinase (PKA) inhibitor fragment 14–22 myristoylated <t>trifluoroacetate</t> salt (PKI[14–22]), 1 μmol/L; exchange factor directly activated by cAMP inhibitor (ESI-09), 6.4 μmol/L; calcium-calmodulin-dependent protein kinase kinase inhibitor (STO-609), 10 μmol/L; AMP-activated protein kinase (AMPK) inhibitor (dorsomorphine), 10 μmol/L; Akt inhibitor 10-(4′-[[ N -diethylamino]]butyl)-2-chlorophenoxazine (AktI X), 5 μmol/L; NOS inhibitor ( l -NAME), 1 mmol/L; a effects of liraglutide and the Ex-9 GLP-1R antagonist on endothelial NO production, 2 h after stimulation; b effects of inhibitors of downstream molecules of GLP-1R on liraglutide-stimulated NO production; n = 4–6; *p
    Drugs Damgo, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Millipore damgo d ala2 n me phe4 gly5 ol enkephalin acetate salt
    Unilateral dialysis during the day of <t>100μM</t> <t>DAMGO</t> (n=9, filled circles) did not significantly ( P ≥0.758) alter ventilation (V̇ I , panel A), breathing frequency (f, panel B) or tidal volume (V T , panel C) compared to dialysis of mCSF alone (n=7, open circles). Data are means ± SE. The x Axis is time from start of 180 minutes of dialysis. As indicated by the black line, 100μM DAMGO was dialyzed between 60 and 120 minutes. The values shown during and after DAMGO dialyses are the percent of the last 15 minutes prior to DAMGO dialyses. F and P values are the interaction term obtained from two-way repeated measures ANOVA using time and dose as factors. Note the trend of a transient reduction in V̇ I and f over the last 30 minutes of DAMGO dialysis.
    Damgo D Ala2 N Me Phe4 Gly5 Ol Enkephalin Acetate Salt, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Hello Bio Inc damgo
    Unilateral dialysis during the day of <t>100μM</t> <t>DAMGO</t> (n=9, filled circles) did not significantly ( P ≥0.758) alter ventilation (V̇ I , panel A), breathing frequency (f, panel B) or tidal volume (V T , panel C) compared to dialysis of mCSF alone (n=7, open circles). Data are means ± SE. The x Axis is time from start of 180 minutes of dialysis. As indicated by the black line, 100μM DAMGO was dialyzed between 60 and 120 minutes. The values shown during and after DAMGO dialyses are the percent of the last 15 minutes prior to DAMGO dialyses. F and P values are the interaction term obtained from two-way repeated measures ANOVA using time and dose as factors. Note the trend of a transient reduction in V̇ I and f over the last 30 minutes of DAMGO dialysis.
    Damgo, supplied by Hello Bio Inc, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Phoenix Pharmaceuticals damgo
    <t>Endothelin</t> effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the <t>DAMGO</t> activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.
    Damgo, supplied by Phoenix Pharmaceuticals, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    American Radiolabeled Chemicals Inc h damgo
    <t>Endothelin</t> effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the <t>DAMGO</t> activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.
    H Damgo, supplied by American Radiolabeled Chemicals Inc, used in various techniques. Bioz Stars score: 89/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    PolyPeptide Laboratories h damgo
    <t>Endothelin</t> effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the <t>DAMGO</t> activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.
    H Damgo, supplied by PolyPeptide Laboratories, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    PerkinElmer net902250uc
    <t>Endothelin</t> effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the <t>DAMGO</t> activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.
    Net902250uc, supplied by PerkinElmer, used in various techniques. Bioz Stars score: 92/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Millipore antibodies damgo
    <t>Endothelin</t> effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the <t>DAMGO</t> activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.
    Antibodies Damgo, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore reagents damgo
    <t>Endothelin</t> effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the <t>DAMGO</t> activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.
    Reagents Damgo, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Merck & Co damgo acetate salt
    Membrane potential regulates μ receptor‐induced K ir 3.X currents in <t>HEK293T</t> cells. (a) Representative recording (out of n = 6) of inward K + currents in HEK293T cells expressing wild‐type μ receptors (MOP‐wt) and K ir 3.X channels is shown. K ir 3.X currents were evoked by 4.5 nM morphine (Mor) and 30 nM <t>DAMGO</t> and measured at −90 and −20 mV (voltage protocol is depicted at the bottom; note that depolarization to −20 mV shifts both basal and active currents due to the current–voltage relationship [see Figure S1 ] of the channel). Levels that were used for calculation of maximum responses are shown as light grey line (−90 mV) or dark grey line (−20 mV), and amplitude height is shown by boxes (morphine response: filled box; maximum DAMGO response: empty box). (b) K ir 3.X current responses evoked by non‐saturating morphine concentrations were normalized to the maximum response (evoked by a saturating DAMGO concentration) at respective membrane potentials ( n = 6, for further explanation of evaluation, see Section 2 ). (c) Representative recording (out of n = 7) of inward K + currents. K ir 3.X currents were evoked by 3 nM morphine and 30 nM DAMGO and measured and evaluated as explained in (a) (non‐saturating DAMGO response: filled box; saturating response: empty box). (d) K ir 3.X current responses evoked by non‐saturating DAMGO concentrations were normalized to the maximum response (evoked by a saturating DAMGO concentration) at respective membrane potentials ( n = 7, for further explanation of evaluation, see Section 2 ). Responses at −90 and −20 mV were compared in the same recording. * P
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    Image Search Results


    Histological analysis of microinfusion sites for both the muscimol and DAMGO injections. A , Nucleus accumbens placements of one representative study. The remaining slides display the placements of all subjects for each respective study. B , Dorsomedial hypothalamus, lateral hypothalamus, dorsal hippocampus ( C ), ventral tegmental area, ( D .

    Journal: The Journal of Neuroscience

    Article Title: Nucleus Accumbens μ-Opioids Regulate Intake of a High-Fat Diet via Activation of a Distributed Brain Network

    doi: 10.1523/JNEUROSCI.23-07-02882.2003

    Figure Lengend Snippet: Histological analysis of microinfusion sites for both the muscimol and DAMGO injections. A , Nucleus accumbens placements of one representative study. The remaining slides display the placements of all subjects for each respective study. B , Dorsomedial hypothalamus, lateral hypothalamus, dorsal hippocampus ( C ), ventral tegmental area, ( D .

    Article Snippet: DAMGO (Research Biochemicals, Natick, MA) and muscimol (Sigma) were both dissolved in sterile 0.9% saline.

    Techniques:

    Feeding response to accumbens μ-opioid stimulation (250 ng DAMGO) after muscimol inactivation of selected structures. Values represent group means (±SEM). ∗, DAMGO/SAL versus DAMGO/MUSC; +, DAMGO/SAL versus SAL/SAL; #, MUSC/SAL versus SAL/SAL. Level of significance is shown by number of symbols (* p

    Journal: The Journal of Neuroscience

    Article Title: Nucleus Accumbens μ-Opioids Regulate Intake of a High-Fat Diet via Activation of a Distributed Brain Network

    doi: 10.1523/JNEUROSCI.23-07-02882.2003

    Figure Lengend Snippet: Feeding response to accumbens μ-opioid stimulation (250 ng DAMGO) after muscimol inactivation of selected structures. Values represent group means (±SEM). ∗, DAMGO/SAL versus DAMGO/MUSC; +, DAMGO/SAL versus SAL/SAL; #, MUSC/SAL versus SAL/SAL. Level of significance is shown by number of symbols (* p

    Article Snippet: DAMGO (Research Biochemicals, Natick, MA) and muscimol (Sigma) were both dissolved in sterile 0.9% saline.

    Techniques:

    Selective and non-specific binding for MOR and KOR autoradiography. 1A) Selective binding of MOR using [ 3 H]DAMGO blocking DOR and KOR by co-incubating with DPDPE and U69,593, respectively 1B) Non-specific binding of MOR with [ 3 H]DAMGO and co-incubating

    Journal: Neuroscience

    Article Title: μ and κ Opioid receptor distribution in the monogamous titi monkey (Callicebus cupreus): Implications for social behavior and endocrine functioning

    doi: 10.1016/j.neuroscience.2015.01.023

    Figure Lengend Snippet: Selective and non-specific binding for MOR and KOR autoradiography. 1A) Selective binding of MOR using [ 3 H]DAMGO blocking DOR and KOR by co-incubating with DPDPE and U69,593, respectively 1B) Non-specific binding of MOR with [ 3 H]DAMGO and co-incubating

    Article Snippet: Sections were dipped in Tris buffer (50mM Tris base; pH 7.4) for 60 minutes at room temperature then incubated for 90 minutes in 3.0 nM [3 H]U69,593 (PerkinElmer, Inc., Boston, MA) and co-incubated with 400nM of DPDPE and 400nM DAMGO (Tocris Bioscience, Minneapolis, MN) at room temperature to block DOR and MOR, respectively.

    Techniques: Binding Assay, Autoradiography, Blocking Assay

    Spinal μ-opioid receptor (MOR) activation reduces nociceptive responses in all ages. (A) Typical electromyographic (EMG) traces in postnatal day (P)10, P21, and adult rats during baseline (without any stimulation), predrug (a typical threshold response before application of drug) and postdrug (A: DAMGO 30 ng; B: CTOP 120 ng) periods. The application of MOR opioid agonist DAMGO onto the spinal cord produced antinociceptive responses in all ages tested. Spinal reflex excitability (C) was decreased when compared to age-matched saline and predrug responses in all ages, both saline and CTOP had no significant effect. Mechanical threshold (D) was increased when DAMGO was administered in P10 and P21 rats. ++ , ++++ P

    Journal: Pain

    Article Title: Postnatal maturation of endogenous opioid systems within the periaqueductal grey and spinal dorsal horn of the rat

    doi: 10.1016/j.pain.2013.09.022

    Figure Lengend Snippet: Spinal μ-opioid receptor (MOR) activation reduces nociceptive responses in all ages. (A) Typical electromyographic (EMG) traces in postnatal day (P)10, P21, and adult rats during baseline (without any stimulation), predrug (a typical threshold response before application of drug) and postdrug (A: DAMGO 30 ng; B: CTOP 120 ng) periods. The application of MOR opioid agonist DAMGO onto the spinal cord produced antinociceptive responses in all ages tested. Spinal reflex excitability (C) was decreased when compared to age-matched saline and predrug responses in all ages, both saline and CTOP had no significant effect. Mechanical threshold (D) was increased when DAMGO was administered in P10 and P21 rats. ++ , ++++ P

    Article Snippet: Drugs DAMGO (MOR-agonist, 30 ng; Tocris, Abingdon, Oxon, UK) and CTOP (MOR-antagonist, 100 ng; Tocris) were administered at doses determined from previously published studies in adult brainstem .

    Techniques: Activation Assay, Produced

    Recruitment of β-arrestin2 by activation of μ-opioid receptors. Stably transfected HEK293 cells coexpressing μ-opioid receptors and β-arrestin2 were pretreated for 60 min with DAMGO or PnPP-19 at the indicated concentrations. The group “DAMGO + PnPP-19” represents prior incubation of the cells with 10 μM of PnPP-19 for 30 min. β-arrestin2 recruitment was quantified by high content imaging complementation assay as described in Materials and Methods ( n = 5).

    Journal: Toxins

    Article Title: The Peptide PnPP-19, a Spider Toxin Derivative, Activates μ-Opioid Receptors and Modulates Calcium Channels

    doi: 10.3390/toxins10010043

    Figure Lengend Snippet: Recruitment of β-arrestin2 by activation of μ-opioid receptors. Stably transfected HEK293 cells coexpressing μ-opioid receptors and β-arrestin2 were pretreated for 60 min with DAMGO or PnPP-19 at the indicated concentrations. The group “DAMGO + PnPP-19” represents prior incubation of the cells with 10 μM of PnPP-19 for 30 min. β-arrestin2 recruitment was quantified by high content imaging complementation assay as described in Materials and Methods ( n = 5).

    Article Snippet: Plates were kept in a humidified incubator at 37 °C filled with 5% CO2 for 24 h. HEK293T were stimulated with the selective opioid agonist DAMGO (Tocris, Minneapolis, MN, USA) or the synthetic peptide PnPP-19 in HEPES-buffered saline solution (HBSS) including 0.1% v / v BSA (10−10 M–10−4 M) for 60 min at 37 °C.

    Techniques: Activation Assay, Stable Transfection, Transfection, Incubation, Imaging

    Relative efficacy values for DAMGO, etorphine, endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3

    Journal: Molecular Pharmacology

    Article Title: Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor

    doi: 10.1124/mol.112.078659

    Figure Lengend Snippet: Relative efficacy values for DAMGO, etorphine, endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3

    Article Snippet: Morphine hydrochloride was obtained from Mcfarlan Smith (Edinburgh, UK), etorphine from Research Triangle Institute (Research Triangle Park, NC), and DAMGO from Bachem (Bubendorf, Switzerland).

    Techniques: Binding Assay

    Concentration-response curves for activation of the GIRK current in rat LC neurons by DAMGO, etorphine, and endomorphin-2. In individual LC neurons, concentration-response curves for DAMGO ( n = 3–5) (A), etorphine ( n = 3–8) (B),and endomorphin-2

    Journal: Molecular Pharmacology

    Article Title: Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor

    doi: 10.1124/mol.112.078659

    Figure Lengend Snippet: Concentration-response curves for activation of the GIRK current in rat LC neurons by DAMGO, etorphine, and endomorphin-2. In individual LC neurons, concentration-response curves for DAMGO ( n = 3–5) (A), etorphine ( n = 3–8) (B),and endomorphin-2

    Article Snippet: Morphine hydrochloride was obtained from Mcfarlan Smith (Edinburgh, UK), etorphine from Research Triangle Institute (Research Triangle Park, NC), and DAMGO from Bachem (Bubendorf, Switzerland).

    Techniques: Concentration Assay, Activation Assay

    Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of MOR-flox mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of MOR-flox mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM

    Article Snippet: Reagents The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Slice Preparation, Mouse Assay, Plasmid Preparation, Injection, Infection, Expressing, Knock-Out

    mOP-LTD occurs at anterior insular cortex inputs to DLS and is ethanol sensitive. a Schematic figure of the injection paradigm enabling optogenetic recording from C57BL/6J DLS MSNs. An AAV vector coding for ChR2 (AAV.hSyn.ChR2) was injected 14 days prior to recordings. Coronal brain slices showing the infection of anterior insular cortex sending projections to the DLS and nucleus accumbens. Bar scales: +2.4, 200 μm; +1.7, 1000 μm; +1.2, 1000 μm; +0.1, 1000 μm. b Representative light-evoked synaptic traces from the DLS before and after DAMGO (0.3 μM, 5 min) and blocked with MOR antagonist CTAP (1 μM). c , d DAMGO application induced mOP-LTD at anterior insular terminals in the DLS and this MOR-mediated LTD was blocked by the application of CTAP ( P = 0.027, t 13 = 2.49, Control: n = 9 from 3 mice; CTAP: n = 6 from 2 mice). e Representative oEPSC traces from the DLS before and after DAMGO (0.3 μM, 5 min) application in saline (blue traces) and EtOH (red traces)-injected C57BL/6J mice. f , g EtOH exposure produced a disruption of mOP-LTD from anterior insular inputs induced by DAMGO (0.3 μM, 5 min) in the DLS ( P = 0.0046, t 9 = 3.75; Saline: n = 6 from 2 mice; EtOH: n = 5 from 3 mice). Unpaired Student’s t test. * P

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: mOP-LTD occurs at anterior insular cortex inputs to DLS and is ethanol sensitive. a Schematic figure of the injection paradigm enabling optogenetic recording from C57BL/6J DLS MSNs. An AAV vector coding for ChR2 (AAV.hSyn.ChR2) was injected 14 days prior to recordings. Coronal brain slices showing the infection of anterior insular cortex sending projections to the DLS and nucleus accumbens. Bar scales: +2.4, 200 μm; +1.7, 1000 μm; +1.2, 1000 μm; +0.1, 1000 μm. b Representative light-evoked synaptic traces from the DLS before and after DAMGO (0.3 μM, 5 min) and blocked with MOR antagonist CTAP (1 μM). c , d DAMGO application induced mOP-LTD at anterior insular terminals in the DLS and this MOR-mediated LTD was blocked by the application of CTAP ( P = 0.027, t 13 = 2.49, Control: n = 9 from 3 mice; CTAP: n = 6 from 2 mice). e Representative oEPSC traces from the DLS before and after DAMGO (0.3 μM, 5 min) application in saline (blue traces) and EtOH (red traces)-injected C57BL/6J mice. f , g EtOH exposure produced a disruption of mOP-LTD from anterior insular inputs induced by DAMGO (0.3 μM, 5 min) in the DLS ( P = 0.0046, t 9 = 3.75; Saline: n = 6 from 2 mice; EtOH: n = 5 from 3 mice). Unpaired Student’s t test. * P

    Article Snippet: Reagents The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Injection, Plasmid Preparation, Infection, Mouse Assay, Produced

    MOR activation produces LTD of excitatory transmission in the dorsal striatum. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the dorsolateral striatum (DLS) of C57BL/6J mice. b Representative electrically evoked synaptic traces at baseline and after DAMGO (0.3 μM, 5 min) application. c DAMGO induced mOP-LTD of eEPSC amplitude in DLS MSNs of C57BL/6J mice ( n = 7 slices from 4 mice). d The presence of mOP-LTD is not related to alterations in series resistance. e Schematic figure of coronal brain slice showing the recording of eEPSCs by focal electric stimulation in the dorsomedial striatum (DMS). f Representative electrically evoked synaptic traces before and after DAMGO (0.3 μM, 5 min) application. g The activation of MOR by DAMGO induced LTD of eEPSC amplitude in DMS MSNs of C57BL/6J ( n = 6 from 2 mice). h The series resistance was stable during DMS recordings. Data represent mean ± SEM

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: MOR activation produces LTD of excitatory transmission in the dorsal striatum. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the dorsolateral striatum (DLS) of C57BL/6J mice. b Representative electrically evoked synaptic traces at baseline and after DAMGO (0.3 μM, 5 min) application. c DAMGO induced mOP-LTD of eEPSC amplitude in DLS MSNs of C57BL/6J mice ( n = 7 slices from 4 mice). d The presence of mOP-LTD is not related to alterations in series resistance. e Schematic figure of coronal brain slice showing the recording of eEPSCs by focal electric stimulation in the dorsomedial striatum (DMS). f Representative electrically evoked synaptic traces before and after DAMGO (0.3 μM, 5 min) application. g The activation of MOR by DAMGO induced LTD of eEPSC amplitude in DMS MSNs of C57BL/6J ( n = 6 from 2 mice). h The series resistance was stable during DMS recordings. Data represent mean ± SEM

    Article Snippet: Reagents The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Activation Assay, Transmission Assay, Slice Preparation, Mouse Assay

    Morphine inhibits IPSCs through activation of MOPs and DOPs. ( A ) Exemplar recording of the inhibition of sIPSC frequency by morphine (100 μM) in a VTA neuron, with the associated graph of cumulative probability of the inter-event intervals. ( B ) Graph of the concentration-dependent inhibition of sIPSC frequency by morphine in WT neurons (EC 50 = 2 µM (95% CIs = 0.54 and 7.2 µM), slope = 0.8, n = 5–10) and MOP+/− neurons (EC 50 = 128 µM, (95% CIs = 20 and 826 µM), slope = 0.7, n = 4–8). ( C ) Bar graph of the average inhibition by morphine (100 μM) of sIPSC frequency in WT (72 ± 5%, n = 7), MOP+/− (50 ± 9%, n = 4) and MOP−/− (11 ± 5%, n = 7) neurons. ( D ) Exemplar sIPSCs recorded from a WT neuron in the absence and presence of DPDPE (1 µM), with the associated graph of cumulative probabilities. ( E ) Exemplar recording from a MOP−/− neuron in the absence and presence of DPDPE, with the graph of cumulative probability. ( F ) Bar graph illustrating the average inhibition by DPDPE of sIPSC frequency in WT (37 ± 7%, n = 6), MOP−/− (34 ± 2%. n = 5) and DOP−/− neurons (7 ± 5%, n = 6). ( G ) sIPSCs recorded from a DOP−/− VTA neuron, illustrating the remaining inhibition by morphine, with the associated graph of cumulative probability. ( H ) Bar graph of inhibition of sIPSC frequency by morphine and DAMGO. Inhibition by morphine was reduced in DOP−/− neurons (42 ± 5%, n = 8) compared to WT neurons (64 ± 5, n = 10; unpaired t test p = 0.004; see Table 1 ). While Inhibition by DAMGO (42 ± 11%, n = 8) was not significantly different (unpaired t test p = 0.31, WT n = 7, DOP−/− n = 7) to WT (55 ± 4%, n = 7). Vertical lines represent ± SEM. One way ANOVA p

    Journal: Scientific Reports

    Article Title: Morphine activation of mu opioid receptors causes disinhibition of neurons in the ventral tegmental area mediated by β-arrestin2 and c-Src

    doi: 10.1038/s41598-017-10360-8

    Figure Lengend Snippet: Morphine inhibits IPSCs through activation of MOPs and DOPs. ( A ) Exemplar recording of the inhibition of sIPSC frequency by morphine (100 μM) in a VTA neuron, with the associated graph of cumulative probability of the inter-event intervals. ( B ) Graph of the concentration-dependent inhibition of sIPSC frequency by morphine in WT neurons (EC 50 = 2 µM (95% CIs = 0.54 and 7.2 µM), slope = 0.8, n = 5–10) and MOP+/− neurons (EC 50 = 128 µM, (95% CIs = 20 and 826 µM), slope = 0.7, n = 4–8). ( C ) Bar graph of the average inhibition by morphine (100 μM) of sIPSC frequency in WT (72 ± 5%, n = 7), MOP+/− (50 ± 9%, n = 4) and MOP−/− (11 ± 5%, n = 7) neurons. ( D ) Exemplar sIPSCs recorded from a WT neuron in the absence and presence of DPDPE (1 µM), with the associated graph of cumulative probabilities. ( E ) Exemplar recording from a MOP−/− neuron in the absence and presence of DPDPE, with the graph of cumulative probability. ( F ) Bar graph illustrating the average inhibition by DPDPE of sIPSC frequency in WT (37 ± 7%, n = 6), MOP−/− (34 ± 2%. n = 5) and DOP−/− neurons (7 ± 5%, n = 6). ( G ) sIPSCs recorded from a DOP−/− VTA neuron, illustrating the remaining inhibition by morphine, with the associated graph of cumulative probability. ( H ) Bar graph of inhibition of sIPSC frequency by morphine and DAMGO. Inhibition by morphine was reduced in DOP−/− neurons (42 ± 5%, n = 8) compared to WT neurons (64 ± 5, n = 10; unpaired t test p = 0.004; see Table 1 ). While Inhibition by DAMGO (42 ± 11%, n = 8) was not significantly different (unpaired t test p = 0.31, WT n = 7, DOP−/− n = 7) to WT (55 ± 4%, n = 7). Vertical lines represent ± SEM. One way ANOVA p

    Article Snippet: Drug application Spontaneous inhibitory postsynaptic currents (sIPSC) were recorded in the absence and presence of a variety of drugs including bicuculline, morphine, DAMGO, DPDPE (Abcam, Cambridge, UK), PP2, PP3 and SL327 (all from Tocris, Bristol, UK).

    Techniques: Activation Assay, Inhibition, Concentration Assay

    Liraglutide stimulated NO production via the cAMP/PKA/AMPK/eNOS pathway in HUVECs. NO production by HUVECs was determined by measuring levels of the stable metabolites of NO (NO 2 and NO 3 ) in the culture medium. HUVECs were stimulated with the indicated concentrations of agents (saline or liraglutide 0.1–100 nmol/L) for 2 h, following serum starvation in M199, 0.3% FBS, for 1 h. Inhibitors were added 30 min prior to stimulation at the following concentrations: GLP-1R antagonist exendin-(9–39) (Ex-9), 100 nmol/L; cAMP inhibitor SQ22536 (SQ), 100 μmol/L; cAMP-dependent protein kinase (PKA) inhibitor fragment 14–22 myristoylated trifluoroacetate salt (PKI[14–22]), 1 μmol/L; exchange factor directly activated by cAMP inhibitor (ESI-09), 6.4 μmol/L; calcium-calmodulin-dependent protein kinase kinase inhibitor (STO-609), 10 μmol/L; AMP-activated protein kinase (AMPK) inhibitor (dorsomorphine), 10 μmol/L; Akt inhibitor 10-(4′-[[ N -diethylamino]]butyl)-2-chlorophenoxazine (AktI X), 5 μmol/L; NOS inhibitor ( l -NAME), 1 mmol/L; a effects of liraglutide and the Ex-9 GLP-1R antagonist on endothelial NO production, 2 h after stimulation; b effects of inhibitors of downstream molecules of GLP-1R on liraglutide-stimulated NO production; n = 4–6; *p

    Journal: Cardiovascular Diabetology

    Article Title: The role of endothelial nitric oxide in the anti-restenotic effects of liraglutide in a mouse model of restenosis

    doi: 10.1186/s12933-017-0603-x

    Figure Lengend Snippet: Liraglutide stimulated NO production via the cAMP/PKA/AMPK/eNOS pathway in HUVECs. NO production by HUVECs was determined by measuring levels of the stable metabolites of NO (NO 2 and NO 3 ) in the culture medium. HUVECs were stimulated with the indicated concentrations of agents (saline or liraglutide 0.1–100 nmol/L) for 2 h, following serum starvation in M199, 0.3% FBS, for 1 h. Inhibitors were added 30 min prior to stimulation at the following concentrations: GLP-1R antagonist exendin-(9–39) (Ex-9), 100 nmol/L; cAMP inhibitor SQ22536 (SQ), 100 μmol/L; cAMP-dependent protein kinase (PKA) inhibitor fragment 14–22 myristoylated trifluoroacetate salt (PKI[14–22]), 1 μmol/L; exchange factor directly activated by cAMP inhibitor (ESI-09), 6.4 μmol/L; calcium-calmodulin-dependent protein kinase kinase inhibitor (STO-609), 10 μmol/L; AMP-activated protein kinase (AMPK) inhibitor (dorsomorphine), 10 μmol/L; Akt inhibitor 10-(4′-[[ N -diethylamino]]butyl)-2-chlorophenoxazine (AktI X), 5 μmol/L; NOS inhibitor ( l -NAME), 1 mmol/L; a effects of liraglutide and the Ex-9 GLP-1R antagonist on endothelial NO production, 2 h after stimulation; b effects of inhibitors of downstream molecules of GLP-1R on liraglutide-stimulated NO production; n = 4–6; *p

    Article Snippet: Chemical agents The chemical agents were purchased as follows: liraglutide from Novo Nordisk Japan (Chiyoda, Tokyo, Japan); exendin-(9–39) (Ex-9) from AnaSpec (Fremont, CA, USA); l -NAME, SQ22536 (SQ), cAMP-dependent protein kinase (PKA) inhibitor fragment 14–22 myristoylated trifluoroacetate salt (PKI[14–22]), ESI-09, STO-609, and N -omega-nitro-l -arginine methyl ester (l -NAME) from Sigma-Aldrich Japan (Shinagawa, Tokyo, Japan); 10-(4′-[[N -diethylamino]]butyl)-2-chlorophenoxazine (Akt inhibitor X) was purchased from Santa Cruz (Dallas, Texas, USA) and dorsomorphin dihydrochloride from Wako (Osaka, Osaka, Japan).

    Techniques:

    Unilateral dialysis during the day of 100μM DAMGO (n=9, filled circles) did not significantly ( P ≥0.758) alter ventilation (V̇ I , panel A), breathing frequency (f, panel B) or tidal volume (V T , panel C) compared to dialysis of mCSF alone (n=7, open circles). Data are means ± SE. The x Axis is time from start of 180 minutes of dialysis. As indicated by the black line, 100μM DAMGO was dialyzed between 60 and 120 minutes. The values shown during and after DAMGO dialyses are the percent of the last 15 minutes prior to DAMGO dialyses. F and P values are the interaction term obtained from two-way repeated measures ANOVA using time and dose as factors. Note the trend of a transient reduction in V̇ I and f over the last 30 minutes of DAMGO dialysis.

    Journal: Respiratory physiology & neurobiology

    Article Title: Effects on breathing of agonists to μ-opioid or GABAA receptors dialyzed into the Ventral Respiratory Column of awake and sleeping goats

    doi: 10.1016/j.resp.2017.01.007

    Figure Lengend Snippet: Unilateral dialysis during the day of 100μM DAMGO (n=9, filled circles) did not significantly ( P ≥0.758) alter ventilation (V̇ I , panel A), breathing frequency (f, panel B) or tidal volume (V T , panel C) compared to dialysis of mCSF alone (n=7, open circles). Data are means ± SE. The x Axis is time from start of 180 minutes of dialysis. As indicated by the black line, 100μM DAMGO was dialyzed between 60 and 120 minutes. The values shown during and after DAMGO dialyses are the percent of the last 15 minutes prior to DAMGO dialyses. F and P values are the interaction term obtained from two-way repeated measures ANOVA using time and dose as factors. Note the trend of a transient reduction in V̇ I and f over the last 30 minutes of DAMGO dialysis.

    Article Snippet: During studies, the perfusate was either mock cerebral spinal fluid (mCSF: 124mM NaCl, 2.0mM KCL, 2.0mM MgCl2 , 1.3mM K2 PO4 , 2.0mM CaCl2 , 11mM glucose, 26mM NaHCO3 − and pH 7.32 in sterile distilled H2O) alone or with the μ-opioid agonist DAMGO (10, 50 or 100μM, Sigma-Aldrich: E7384) or the GABAA agonist muscimol (0.5, 1.0, or 10.0mM, Abcam: ab120094).

    Techniques:

    Visual inspection of ventilatory tracings indicates variability of breathing increased and inspiratory time decreased during and after bilateral dialysis of 100μM DAMGO. The four tracings were from a single goat for a portion of the last 15 minutes of the predialysis control period (panel A) and the last 15 minutes of each of three hours of mCSF dialysis (panels B-D) with DAMGO increased during the second of the three hours (Panel C).

    Journal: Respiratory physiology & neurobiology

    Article Title: Effects on breathing of agonists to μ-opioid or GABAA receptors dialyzed into the Ventral Respiratory Column of awake and sleeping goats

    doi: 10.1016/j.resp.2017.01.007

    Figure Lengend Snippet: Visual inspection of ventilatory tracings indicates variability of breathing increased and inspiratory time decreased during and after bilateral dialysis of 100μM DAMGO. The four tracings were from a single goat for a portion of the last 15 minutes of the predialysis control period (panel A) and the last 15 minutes of each of three hours of mCSF dialysis (panels B-D) with DAMGO increased during the second of the three hours (Panel C).

    Article Snippet: During studies, the perfusate was either mock cerebral spinal fluid (mCSF: 124mM NaCl, 2.0mM KCL, 2.0mM MgCl2 , 1.3mM K2 PO4 , 2.0mM CaCl2 , 11mM glucose, 26mM NaHCO3 − and pH 7.32 in sterile distilled H2O) alone or with the μ-opioid agonist DAMGO (10, 50 or 100μM, Sigma-Aldrich: E7384) or the GABAA agonist muscimol (0.5, 1.0, or 10.0mM, Abcam: ab120094).

    Techniques:

    Endothelin effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the DAMGO activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.

    Journal: The Journal of biological chemistry

    Article Title: Eicosanoids Inhibit the G-protein-gated Inwardly Rectifying Potassium Channel (Kir3) at the Na+/PIP2 Gating Site *

    doi: 10.1074/jbc.M010097200

    Figure Lengend Snippet: Endothelin effects on channel mutants A , diagrams depict channel mutants: Kir3.4 (S143T) parent, N-terminal truncation, and chimeras. We produced the Kir3.4(S143T) using a cDNA template for cRNA coding a Kir3.4(S143T) having a truncated (1–57) N terminus. We used Kir3 chimeras: Kir3.4(S143T)-(1–338)/Kir3.1-(333–501) and Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). B , oocytes were injected with 1 ng of MOR and 1 ng of HETAR, and either 1 ng of Kir3.4(S143T), 1 ng of Kir3.4(S143T)-(Δ1–57), 1 ng of Kir3.4(S143T)-(1–338)/Kir3.1-(333–501), or 1 ng of Kir3.4(S143T)-(1–249)/Kir3.1-(244–501). The percent inhibition of the second mu opioid response after Et-1 pretreatment is shown. The bar graph summarizes the effects of Et-1 on the DAMGO activation of MOR compared with untreated controls from the same batch. Data are means ± S.E. from four to seven oocytes and two to three independent experiments.

    Article Snippet: Endothelin-1 and DAMGO were obtained from Phoenix Pharmaceuticals, Belmont, CA and were stored at −20 °C until use.

    Techniques: Produced, Injection, Inhibition, Activation Assay

    Membrane potential regulates μ receptor‐induced K ir 3.X currents in HEK293T cells. (a) Representative recording (out of n = 6) of inward K + currents in HEK293T cells expressing wild‐type μ receptors (MOP‐wt) and K ir 3.X channels is shown. K ir 3.X currents were evoked by 4.5 nM morphine (Mor) and 30 nM DAMGO and measured at −90 and −20 mV (voltage protocol is depicted at the bottom; note that depolarization to −20 mV shifts both basal and active currents due to the current–voltage relationship [see Figure S1 ] of the channel). Levels that were used for calculation of maximum responses are shown as light grey line (−90 mV) or dark grey line (−20 mV), and amplitude height is shown by boxes (morphine response: filled box; maximum DAMGO response: empty box). (b) K ir 3.X current responses evoked by non‐saturating morphine concentrations were normalized to the maximum response (evoked by a saturating DAMGO concentration) at respective membrane potentials ( n = 6, for further explanation of evaluation, see Section 2 ). (c) Representative recording (out of n = 7) of inward K + currents. K ir 3.X currents were evoked by 3 nM morphine and 30 nM DAMGO and measured and evaluated as explained in (a) (non‐saturating DAMGO response: filled box; saturating response: empty box). (d) K ir 3.X current responses evoked by non‐saturating DAMGO concentrations were normalized to the maximum response (evoked by a saturating DAMGO concentration) at respective membrane potentials ( n = 7, for further explanation of evaluation, see Section 2 ). Responses at −90 and −20 mV were compared in the same recording. * P

    Journal: British Journal of Pharmacology

    Article Title: Voltage modulates the effect of μ‐receptor activation in a ligand‐dependent manner. Voltage modulates the effect of μ‐receptor activation in a ligand‐dependent manner

    doi: 10.1111/bph.15070

    Figure Lengend Snippet: Membrane potential regulates μ receptor‐induced K ir 3.X currents in HEK293T cells. (a) Representative recording (out of n = 6) of inward K + currents in HEK293T cells expressing wild‐type μ receptors (MOP‐wt) and K ir 3.X channels is shown. K ir 3.X currents were evoked by 4.5 nM morphine (Mor) and 30 nM DAMGO and measured at −90 and −20 mV (voltage protocol is depicted at the bottom; note that depolarization to −20 mV shifts both basal and active currents due to the current–voltage relationship [see Figure S1 ] of the channel). Levels that were used for calculation of maximum responses are shown as light grey line (−90 mV) or dark grey line (−20 mV), and amplitude height is shown by boxes (morphine response: filled box; maximum DAMGO response: empty box). (b) K ir 3.X current responses evoked by non‐saturating morphine concentrations were normalized to the maximum response (evoked by a saturating DAMGO concentration) at respective membrane potentials ( n = 6, for further explanation of evaluation, see Section 2 ). (c) Representative recording (out of n = 7) of inward K + currents. K ir 3.X currents were evoked by 3 nM morphine and 30 nM DAMGO and measured and evaluated as explained in (a) (non‐saturating DAMGO response: filled box; saturating response: empty box). (d) K ir 3.X current responses evoked by non‐saturating DAMGO concentrations were normalized to the maximum response (evoked by a saturating DAMGO concentration) at respective membrane potentials ( n = 7, for further explanation of evaluation, see Section 2 ). Responses at −90 and −20 mV were compared in the same recording. * P

    Article Snippet: 2.12 Materials For HEK293T cell experiments, morphine hydrochloride was purchased from Merck, DAMGO acetate salt, [Met5 ]enkephalin acetate salt and fentanyl citrate were purchased from Sigma Aldrich.

    Techniques: Expressing, Concentration Assay

    The observed voltage sensitivity occurs also in physiological K + concentrations . (a) Representative recording ( n = 7) of outward K + currents measured in HEK293T cells expressing wild‐type μ receptors (MOP‐wt) and K ir 3.4 channels. K ir 3.X currents were evoked by 22.5 nM morphine (Mor; non‐saturating, also see Section 2 ) and 30 nM DAMGO (saturating) and measured at −50 and 0 mV. Levels that were used for calculation of maximum responses are depicted as light grey line (−50 mV) or dark grey line (0 mV), and amplitude height is shown by boxes (morphine response: filled box; saturating DAMGO response: empty box). Voltage protocol is depicted at the bottom; note that depolarization steps shift both basal and active currents due to the current–voltage relationship of the channel (see Figure S2 ). (b) K ir 3.X current responses evoked by non‐saturating morphine concentrations were normalized to the maximum DAMGO response at respective membrane potentials ( n = 7, for further explanation of evaluation, see Section 2 ). Responses at −50 and 0 mV were compared in the same recording. * P

    Journal: British Journal of Pharmacology

    Article Title: Voltage modulates the effect of μ‐receptor activation in a ligand‐dependent manner. Voltage modulates the effect of μ‐receptor activation in a ligand‐dependent manner

    doi: 10.1111/bph.15070

    Figure Lengend Snippet: The observed voltage sensitivity occurs also in physiological K + concentrations . (a) Representative recording ( n = 7) of outward K + currents measured in HEK293T cells expressing wild‐type μ receptors (MOP‐wt) and K ir 3.4 channels. K ir 3.X currents were evoked by 22.5 nM morphine (Mor; non‐saturating, also see Section 2 ) and 30 nM DAMGO (saturating) and measured at −50 and 0 mV. Levels that were used for calculation of maximum responses are depicted as light grey line (−50 mV) or dark grey line (0 mV), and amplitude height is shown by boxes (morphine response: filled box; saturating DAMGO response: empty box). Voltage protocol is depicted at the bottom; note that depolarization steps shift both basal and active currents due to the current–voltage relationship of the channel (see Figure S2 ). (b) K ir 3.X current responses evoked by non‐saturating morphine concentrations were normalized to the maximum DAMGO response at respective membrane potentials ( n = 7, for further explanation of evaluation, see Section 2 ). Responses at −50 and 0 mV were compared in the same recording. * P

    Article Snippet: 2.12 Materials For HEK293T cell experiments, morphine hydrochloride was purchased from Merck, DAMGO acetate salt, [Met5 ]enkephalin acetate salt and fentanyl citrate were purchased from Sigma Aldrich.

    Techniques: Expressing