tertiapin  (Alomone Labs)


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    Structured Review

    Alomone Labs tertiapin
    Summary bar graphs showing the effects of <t>tertiapin</t> (10 μ M ) on resting membrane potential (left panel) and acetylcholine (ACh: 1 μ M ; right panel)-induced hyperpolarization in guinea-pig carotid arteries with endothelium,
    Tertiapin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tertiapin/product/Alomone Labs
    Average 85 stars, based on 7 article reviews
    Price from $9.99 to $1999.99
    tertiapin - by Bioz Stars, 2022-08
    85/100 stars

    Images

    1) Product Images from "C-type natriuretic peptide and endothelium-dependent hyperpolarization in the guinea-pig carotid artery"

    Article Title: C-type natriuretic peptide and endothelium-dependent hyperpolarization in the guinea-pig carotid artery

    Journal:

    doi: 10.1038/sj.bjp.0707476

    Summary bar graphs showing the effects of tertiapin (10 μ M ) on resting membrane potential (left panel) and acetylcholine (ACh: 1 μ M ; right panel)-induced hyperpolarization in guinea-pig carotid arteries with endothelium,
    Figure Legend Snippet: Summary bar graphs showing the effects of tertiapin (10 μ M ) on resting membrane potential (left panel) and acetylcholine (ACh: 1 μ M ; right panel)-induced hyperpolarization in guinea-pig carotid arteries with endothelium,

    Techniques Used:

    2) Product Images from "Release of C-type natriuretic peptide accounts for the biological activity of endothelium-derived hyperpolarizing factor"

    Article Title: Release of C-type natriuretic peptide accounts for the biological activity of endothelium-derived hyperpolarizing factor

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.0336365100

    Responses to EDHF and CNP are similarly attenuated by pertussis toxin (PTx) and tertiapin. Shown is relaxation of rat isolated mesenteric artery by ACh (0.001–10 μM; Upper ) and CNP (0.001–1 μM; Lower ) in the absence or presence of HS-142-1 (30 μM), PTx (400 ng/ml), or tertiapin (10 μM). Data are presented as mean ± SEM; n ≥ 5. ***, P
    Figure Legend Snippet: Responses to EDHF and CNP are similarly attenuated by pertussis toxin (PTx) and tertiapin. Shown is relaxation of rat isolated mesenteric artery by ACh (0.001–10 μM; Upper ) and CNP (0.001–1 μM; Lower ) in the absence or presence of HS-142-1 (30 μM), PTx (400 ng/ml), or tertiapin (10 μM). Data are presented as mean ± SEM; n ≥ 5. ***, P

    Techniques Used: Isolation

    Responses to cANF 4–23 are attenuated by barium plus ouabain, PTx, and tertiapin. Shown is relaxation of rat isolated mesenteric artery by cANF 4–23 (0.001–1 μM) in the absence or presence of Ba 2+ (30 μM) plus ouabain (1 mM), PTx (400 ng/ml), or tertiapin (10 μM). Data are presented as mean ± SEM; n ≥ 5. ***, P
    Figure Legend Snippet: Responses to cANF 4–23 are attenuated by barium plus ouabain, PTx, and tertiapin. Shown is relaxation of rat isolated mesenteric artery by cANF 4–23 (0.001–1 μM) in the absence or presence of Ba 2+ (30 μM) plus ouabain (1 mM), PTx (400 ng/ml), or tertiapin (10 μM). Data are presented as mean ± SEM; n ≥ 5. ***, P

    Techniques Used: Isolation

    Responses to SPER-NO are unaffected by barium plus ouabain, PTx, and tertiapin. Relaxation of rat isolated mesenteric artery by SPER-NO (0.01–30 μM) in the absence or presence of Ba 2+ (30 μM) plus ouabain (1 mM), PTx (400 ng/ml), or tertiapin (10 μM). Data are presented as mean ± SEM; n ≥ 5.
    Figure Legend Snippet: Responses to SPER-NO are unaffected by barium plus ouabain, PTx, and tertiapin. Relaxation of rat isolated mesenteric artery by SPER-NO (0.01–30 μM) in the absence or presence of Ba 2+ (30 μM) plus ouabain (1 mM), PTx (400 ng/ml), or tertiapin (10 μM). Data are presented as mean ± SEM; n ≥ 5.

    Techniques Used: Isolation

    3) Product Images from "CANNABINOID-INDUCED HYPERPHAGIA: CORRELATION WITH INHIBITION OF PROOPIOMELANOCORTIN NEURONS?"

    Article Title: CANNABINOID-INDUCED HYPERPHAGIA: CORRELATION WITH INHIBITION OF PROOPIOMELANOCORTIN NEURONS?

    Journal: Physiology & behavior

    doi: 10.1016/j.physbeh.2007.04.028

    A1 , A reversible outward current elicited by the anandamide derivative ACEA in an arcuate neuron from an intact male guinea pig. This outward current was produced by ACEA (1 μM) from a holding potential of −60 mV in the presence of 1 μM TTX. The break in the trace in the upper panel represents the time necessary to conduct a second I/V relationship, and the early stages of ACEA clearance from the slice. A2 , An I/V plot that reveals the ACEA-induced increase in slope conductance as well as the reversal potential (−97 mV) near the Nernst equilibrium potential for K + . The symbols represent the changes in membrane current (ΔI) observed at different membrane voltages (V m ) that were caused by ACEA. The increase in slope conductance estimated by linear regression between −60 −80 mV was (2.75 nS), whereas that between −100 −130 mV was even greater (4.76 nS; rectification ratio: 1.7). B1 , Another example of the CB1 receptor-mediated outward current recorded in an arcuate neuron from a male guinea pig. As with A1 , this reversible, ACEA-induced outward current (12.2 pA at −60 mV) was observed in the presence of 1 μM TTX. The break in the trace represents the time necessary to conduct a second I/V in the presence of drug, as well as the early stages of drug clearance from the slice. B2 , This trace shows the effect of ACEA observed in the presence of the CB1 receptor antagonist AM251 (1 μM). The data was obtained from the same neuron as in B1 . Note that AM251 completely blocked the ACEA-induced outward current. C1 , The GABA B receptor-mediated activation of GIRK in an arcuate neuron from a male guinea pig. This panel shows the reversible, outward current elicited by the GABA B receptor agonist baclofen (100 μM) from a holding potential of −60 mV in the presence of 1 μM TTX. The break in the trace represents the time necessary to complete a second I/V relationship, and the early stages of drug clearance from the slice. C2 , The attenuation in the GABA B receptor-mediated activation of the outward current by the GIRK channel blocker tertiapin in the arcuate neuron shown in C1 . This panel shows the reduction in the reversible, baclofen-induced outward current in the presence of TTX and tertiapin (10 nM). The break in the trace represents the time necessary to complete a second I/V relationship, and the early stages of drug clearance from the slice. D1 , This panel shows an I/V plot revealing the baclofen-induced increase in slope conductance and the reversal potential (−100 mV) that closely approximates the Nernst equilibrium potential for K + . The symbols represent the change in membrane current (ΔI) observed at different membrane voltages (V m ) that were caused by baclofen (solid circles) or by baclofen in the presence of tertiapin (open circles). The slope conductance estimated by linear regression between −60 −80 mV was 2.23 nS, and that observed between −100 −130 mV was even greater (3.78 nS; rectification ratio: 1.7). Tertiapin reduced this baclofen-induced increase in the slope conductance nearly 70% (to 0.7 nS) between −60 −80 mV, and nearly 75% (to 1.00 nS) between −100 −130 mV. D2 , , A bar graph showing the change in slope conductance (Δ g) evoked by CB1 and GABA B receptor activation at different portions of individual I/V plots. Agonist-induced Δ g is estimated by linear regression between −60 −80 mV, and between −100 −130 mV. Columns represent the means and vertical lines 1 S.E.M. of the Δ g caused by 1 μM ACEA (dark columns; n=7) and 100 μM baclofen (gray columns; n=21).
    Figure Legend Snippet: A1 , A reversible outward current elicited by the anandamide derivative ACEA in an arcuate neuron from an intact male guinea pig. This outward current was produced by ACEA (1 μM) from a holding potential of −60 mV in the presence of 1 μM TTX. The break in the trace in the upper panel represents the time necessary to conduct a second I/V relationship, and the early stages of ACEA clearance from the slice. A2 , An I/V plot that reveals the ACEA-induced increase in slope conductance as well as the reversal potential (−97 mV) near the Nernst equilibrium potential for K + . The symbols represent the changes in membrane current (ΔI) observed at different membrane voltages (V m ) that were caused by ACEA. The increase in slope conductance estimated by linear regression between −60 −80 mV was (2.75 nS), whereas that between −100 −130 mV was even greater (4.76 nS; rectification ratio: 1.7). B1 , Another example of the CB1 receptor-mediated outward current recorded in an arcuate neuron from a male guinea pig. As with A1 , this reversible, ACEA-induced outward current (12.2 pA at −60 mV) was observed in the presence of 1 μM TTX. The break in the trace represents the time necessary to conduct a second I/V in the presence of drug, as well as the early stages of drug clearance from the slice. B2 , This trace shows the effect of ACEA observed in the presence of the CB1 receptor antagonist AM251 (1 μM). The data was obtained from the same neuron as in B1 . Note that AM251 completely blocked the ACEA-induced outward current. C1 , The GABA B receptor-mediated activation of GIRK in an arcuate neuron from a male guinea pig. This panel shows the reversible, outward current elicited by the GABA B receptor agonist baclofen (100 μM) from a holding potential of −60 mV in the presence of 1 μM TTX. The break in the trace represents the time necessary to complete a second I/V relationship, and the early stages of drug clearance from the slice. C2 , The attenuation in the GABA B receptor-mediated activation of the outward current by the GIRK channel blocker tertiapin in the arcuate neuron shown in C1 . This panel shows the reduction in the reversible, baclofen-induced outward current in the presence of TTX and tertiapin (10 nM). The break in the trace represents the time necessary to complete a second I/V relationship, and the early stages of drug clearance from the slice. D1 , This panel shows an I/V plot revealing the baclofen-induced increase in slope conductance and the reversal potential (−100 mV) that closely approximates the Nernst equilibrium potential for K + . The symbols represent the change in membrane current (ΔI) observed at different membrane voltages (V m ) that were caused by baclofen (solid circles) or by baclofen in the presence of tertiapin (open circles). The slope conductance estimated by linear regression between −60 −80 mV was 2.23 nS, and that observed between −100 −130 mV was even greater (3.78 nS; rectification ratio: 1.7). Tertiapin reduced this baclofen-induced increase in the slope conductance nearly 70% (to 0.7 nS) between −60 −80 mV, and nearly 75% (to 1.00 nS) between −100 −130 mV. D2 , , A bar graph showing the change in slope conductance (Δ g) evoked by CB1 and GABA B receptor activation at different portions of individual I/V plots. Agonist-induced Δ g is estimated by linear regression between −60 −80 mV, and between −100 −130 mV. Columns represent the means and vertical lines 1 S.E.M. of the Δ g caused by 1 μM ACEA (dark columns; n=7) and 100 μM baclofen (gray columns; n=21).

    Techniques Used: Produced, Activation Assay

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    Alomone Labs tertiapin q
    DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during <t>tertiapin-Q</t> (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.
    Tertiapin Q, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    tertiapin q - by Bioz Stars, 2022-08
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    DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Journal: Frontiers in Pharmacology

    Article Title: Mu-Opioid Receptor Agonist Induces Kir3 Currents in Mouse Peripheral Sensory Neurons – Effects of Nerve Injury

    doi: 10.3389/fphar.2018.01478

    Figure Lengend Snippet: DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Article Snippet: For tertiapin-Q experiments we applied voltage ramps from a holding potential of -40 mV and measured the induced current at -80 mV, based on previously published protocols ( ; ).

    Techniques: Mouse Assay

    DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Journal: Frontiers in Pharmacology

    Article Title: Mu-Opioid Receptor Agonist Induces Kir3 Currents in Mouse Peripheral Sensory Neurons – Effects of Nerve Injury

    doi: 10.3389/fphar.2018.01478

    Figure Lengend Snippet: DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Article Snippet: Discussion In this study, we found that the MOR-selective agonist DAMGO induces potassium currents in DRG neurons of both naïve mice and mice with CCI of the sciatic nerve, which were diminished by barium and tertiapin-Q indicating the involvement of Kir3 channels.

    Techniques: Mouse Assay

    Effects of tertiapin-Q on oxycodone- and morphine-induced K IR 3.1 channel activation in Xenopus oocytes. The data presented are typical recordings of K + channel current by (A) oxycodone and (B) morphine. Representative current responses to oxycodone (100

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on oxycodone- and morphine-induced K IR 3.1 channel activation in Xenopus oocytes. The data presented are typical recordings of K + channel current by (A) oxycodone and (B) morphine. Representative current responses to oxycodone (100

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Activation Assay

    Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques:

    Effects of tertiapin-Q on oxycodone- and morphine-induced antinociceptive effects in the (A) FBC and (B) neuropathic pain models. Groups of mice were treated with tertiapin-Q (30 pmol per mouse, i.c.v.) 10 min before the opioids, and either oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on oxycodone- and morphine-induced antinociceptive effects in the (A) FBC and (B) neuropathic pain models. Groups of mice were treated with tertiapin-Q (30 pmol per mouse, i.c.v.) 10 min before the opioids, and either oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay

    Dose-dependent antinociceptive effects induced by i.t. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Dose-dependent antinociceptive effects induced by i.t. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques:

    Dose-dependent antinociceptive effect induced by i.c.v. administration of fentanyl in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before fentanyl. Fentanyl (0.1–1.7

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Dose-dependent antinociceptive effect induced by i.c.v. administration of fentanyl in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before fentanyl. Fentanyl (0.1–1.7

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Dose-dependent antinociceptive effects induced by i.c.v. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Dose-dependent antinociceptive effects induced by i.c.v. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Effects of tertiapin-Q on oxycodone- and morphine-induced antinociception after i.c.v. administration in mice tail-flick test. Groups of mice were treated with tertiapin-Q (3–30 mol per mouse, i.c.v.) 10 min before the opioids, either oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on oxycodone- and morphine-induced antinociception after i.c.v. administration in mice tail-flick test. Groups of mice were treated with tertiapin-Q (3–30 mol per mouse, i.c.v.) 10 min before the opioids, either oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Expression of GIRK channels in AtT20 cells . Left panel: Currents were measured before (control) and after the addition of somatostatin (200 nM) during voltage steps applied from the holding potential of −40 to −60, −80, and −100 mV. Addition of tertiapin (500 nM) inhibited the current (bottom records). The solid lines represent zero current. Top right panel: I/V relationship for the somatostatin activated current (Som) displayed inward rectification and a reversal potential of −40 mV. Current values were obtained by subtracting the currents by records obtained in the presence of 1 mM BaCl 2 . Each point represents the mean ± SE current (pA/pF) measured in three to five cells. Bottom right panel: dose versus response curve for tertiapin-Q block of the AtT20 cell GIRK current. Each point represents the mean ± SE inhibition obtained from three to six experiments. The calculated IC 50 value for tertiapin-Q block was 60 nM.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting GIRK Channels for the Development of New Therapeutic Agents

    doi: 10.3389/fphar.2011.00064

    Figure Lengend Snippet: Expression of GIRK channels in AtT20 cells . Left panel: Currents were measured before (control) and after the addition of somatostatin (200 nM) during voltage steps applied from the holding potential of −40 to −60, −80, and −100 mV. Addition of tertiapin (500 nM) inhibited the current (bottom records). The solid lines represent zero current. Top right panel: I/V relationship for the somatostatin activated current (Som) displayed inward rectification and a reversal potential of −40 mV. Current values were obtained by subtracting the currents by records obtained in the presence of 1 mM BaCl 2 . Each point represents the mean ± SE current (pA/pF) measured in three to five cells. Bottom right panel: dose versus response curve for tertiapin-Q block of the AtT20 cell GIRK current. Each point represents the mean ± SE inhibition obtained from three to six experiments. The calculated IC 50 value for tertiapin-Q block was 60 nM.

    Article Snippet: Drugs and chemicals Carbachol, somatostatin, and a Na+ , K+ channel modulator kit (catalog # LO2220), containing 68 compounds, were purchased from Sigma-Aldrich Chemical Corp. Tertiapin-Q (synthetic formulation) was obtained from Alomone Labs.

    Techniques: Expressing, Blocking Assay, Inhibition

    Block of GIRK channels by Ba 2+ and tertiapin-Q . Top panel: somatostatin-sensitive fluorescent signal measured in AtT20 cells pretreated for 5 min with either 2 mM BaCl 2 or 500 nM tertiapin-Q. Each point represents the mean ± SE value obtained in six wells in one plate. Bottom panel: dose versus response curve for tertiapin-Q block of the HL-1 cell (carbachol stimulation) or AtT20 cell (somatostatin stimulation) GIRK fluorescent signal. Each point represents the mean ± SE inhibition obtained from three to five experiments. Calculated IC 50 values for tertiapin-Q block were HL-1 cells = 1.4 nM, AtT20 cells = 102 nM.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting GIRK Channels for the Development of New Therapeutic Agents

    doi: 10.3389/fphar.2011.00064

    Figure Lengend Snippet: Block of GIRK channels by Ba 2+ and tertiapin-Q . Top panel: somatostatin-sensitive fluorescent signal measured in AtT20 cells pretreated for 5 min with either 2 mM BaCl 2 or 500 nM tertiapin-Q. Each point represents the mean ± SE value obtained in six wells in one plate. Bottom panel: dose versus response curve for tertiapin-Q block of the HL-1 cell (carbachol stimulation) or AtT20 cell (somatostatin stimulation) GIRK fluorescent signal. Each point represents the mean ± SE inhibition obtained from three to five experiments. Calculated IC 50 values for tertiapin-Q block were HL-1 cells = 1.4 nM, AtT20 cells = 102 nM.

    Article Snippet: Drugs and chemicals Carbachol, somatostatin, and a Na+ , K+ channel modulator kit (catalog # LO2220), containing 68 compounds, were purchased from Sigma-Aldrich Chemical Corp. Tertiapin-Q (synthetic formulation) was obtained from Alomone Labs.

    Techniques: Blocking Assay, Inhibition