tertiapin  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 85

    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 1 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 1 article reviews
    Price from $9.99 to $1999.99
    tertiapin - by Bioz Stars, 2022-07
    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

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 85
    Alomone Labs r tertiapin
    t-ACPD affects 2 distinct potassium currents. A : current-clamp recording from a UBC in acute cerebellar slice. <t>Tertiapin</t> depolarized the cells when delivered on top of t-ACPD, but never reversed the mGluR-induced blockade of firing (although full recovery was always obtained on t-ACPD washout). The plot in B shows the values of UBCs' membrane potential measured in the presence of t-ACPD and in the presence of both t-ACPD and tertiapin (at the time points indicated by the arrows in A ; the values were −96.9 ± 7 mV in t-ACPD and −89.5 ± 5.6 mV in t-ACPD + tertiapin, 7 cells, P
    R Tertiapin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/r tertiapin/product/Alomone Labs
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    r tertiapin - by Bioz Stars, 2022-07
    85/100 stars
      Buy from Supplier

    Image Search Results


    t-ACPD affects 2 distinct potassium currents. A : current-clamp recording from a UBC in acute cerebellar slice. Tertiapin depolarized the cells when delivered on top of t-ACPD, but never reversed the mGluR-induced blockade of firing (although full recovery was always obtained on t-ACPD washout). The plot in B shows the values of UBCs' membrane potential measured in the presence of t-ACPD and in the presence of both t-ACPD and tertiapin (at the time points indicated by the arrows in A ; the values were −96.9 ± 7 mV in t-ACPD and −89.5 ± 5.6 mV in t-ACPD + tertiapin, 7 cells, P

    Journal: Journal of Neurophysiology

    Article Title: Dynamic Metabotropic Control of Intrinsic Firing in Cerebellar Unipolar Brush Cells

    doi: 10.1152/jn.90533.2008

    Figure Lengend Snippet: t-ACPD affects 2 distinct potassium currents. A : current-clamp recording from a UBC in acute cerebellar slice. Tertiapin depolarized the cells when delivered on top of t-ACPD, but never reversed the mGluR-induced blockade of firing (although full recovery was always obtained on t-ACPD washout). The plot in B shows the values of UBCs' membrane potential measured in the presence of t-ACPD and in the presence of both t-ACPD and tertiapin (at the time points indicated by the arrows in A ; the values were −96.9 ± 7 mV in t-ACPD and −89.5 ± 5.6 mV in t-ACPD + tertiapin, 7 cells, P

    Article Snippet: Drugs and chemicals were from Sigma (St. Louis, MO), except 4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride (ZD7288), (2 S )-2-amino-2-[(1 S ,2 S )-2-carboxyxycloprop-1-yl]-3-(xanth-9-yl) propanoic acid , (±)-aminocyclopentane- trans -1,3-dicarboxylic acid (t-ACPD), (2 R ,4 R )-4-aminopyrrolidine-2,4-dicarboxylate [(2 R ,4 R )APDC; Tocris, Ellisville, MO], tetrodotoxin (TTX), and r-tertiapin (cat #RTT250; Alomone Labs, Jerusalem, Israel).

    Techniques:

    Intrinsic firing of UBCs is tertiapin insensitive. A : current-clamp recording from a UBC; bath application of tertiapin did not produce any significant effect on the firing frequency. Trace segments recorded in the absence and in the presence of tertiapin are shown in B on an expanded timescale. The plot in C summarizes the data obtained in 7 UBCs (the firing frequency was 8.5 ± 2 Hz in control and 8.0 ± 1.4 Hz in the presence of tertiapin).

    Journal: Journal of Neurophysiology

    Article Title: Dynamic Metabotropic Control of Intrinsic Firing in Cerebellar Unipolar Brush Cells

    doi: 10.1152/jn.90533.2008

    Figure Lengend Snippet: Intrinsic firing of UBCs is tertiapin insensitive. A : current-clamp recording from a UBC; bath application of tertiapin did not produce any significant effect on the firing frequency. Trace segments recorded in the absence and in the presence of tertiapin are shown in B on an expanded timescale. The plot in C summarizes the data obtained in 7 UBCs (the firing frequency was 8.5 ± 2 Hz in control and 8.0 ± 1.4 Hz in the presence of tertiapin).

    Article Snippet: Drugs and chemicals were from Sigma (St. Louis, MO), except 4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride (ZD7288), (2 S )-2-amino-2-[(1 S ,2 S )-2-carboxyxycloprop-1-yl]-3-(xanth-9-yl) propanoic acid , (±)-aminocyclopentane- trans -1,3-dicarboxylic acid (t-ACPD), (2 R ,4 R )-4-aminopyrrolidine-2,4-dicarboxylate [(2 R ,4 R )APDC; Tocris, Ellisville, MO], tetrodotoxin (TTX), and r-tertiapin (cat #RTT250; Alomone Labs, Jerusalem, Israel).

    Techniques:

    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,

    Journal:

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

    doi: 10.1038/sj.bjp.0707476

    Figure Lengend 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,

    Article Snippet: Following drugs were used: acetylcholine, indomethacin, N G -nitro- L -arginine, phenylephrine, glibenclamide, levcromakalim, sodium nitroprusside and thiorphan (Sigma, La Verpillère, France); charybdotoxin and apamin (Latoxan, Valence, France); atrial natriuretic peptide (ANP), and CNP (Calbiochem, VWR, Fontenay/bois, France); tertiapin (Alomone labs, Jerusalem, Israel).

    Techniques:

    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

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

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

    doi: 10.1073/pnas.0336365100

    Figure Lengend 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

    Article Snippet: All drugs used were obtained from Sigma except apamin (Calbiochem), cANF4–23 (Peninsula Labs, San Carlos, CA), CNP (Calbiochem), CTx (Calbiochem), HS-142-1 (kind gift of Matsuda, Kyowa Hakko Kogyo, Tokyo), tertiapin (Alomone Labs, Jerusalem), and U-46619 (Biomol, Plymouth Meeting, PA).

    Techniques: 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

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

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

    doi: 10.1073/pnas.0336365100

    Figure Lengend 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

    Article Snippet: All drugs used were obtained from Sigma except apamin (Calbiochem), cANF4–23 (Peninsula Labs, San Carlos, CA), CNP (Calbiochem), CTx (Calbiochem), HS-142-1 (kind gift of Matsuda, Kyowa Hakko Kogyo, Tokyo), tertiapin (Alomone Labs, Jerusalem), and U-46619 (Biomol, Plymouth Meeting, PA).

    Techniques: 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.

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

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

    doi: 10.1073/pnas.0336365100

    Figure Lengend 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.

    Article Snippet: All drugs used were obtained from Sigma except apamin (Calbiochem), cANF4–23 (Peninsula Labs, San Carlos, CA), CNP (Calbiochem), CTx (Calbiochem), HS-142-1 (kind gift of Matsuda, Kyowa Hakko Kogyo, Tokyo), tertiapin (Alomone Labs, Jerusalem), and U-46619 (Biomol, Plymouth Meeting, PA).

    Techniques: Isolation

    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).

    Journal: Physiology & behavior

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

    doi: 10.1016/j.physbeh.2007.04.028

    Figure Lengend 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).

    Article Snippet: Stock solutions of 6-imino-3-(4-methoxyphenyl)-1(6H)-pyridazinebutanoic acid hydrobromide (SR 95531; 10 mM) and tertiapin (1 μM; Alomone Labs) were prepared with UltraPure H2 O. Baclofen (40 mM) was dissolved in 0.1 N HCl.

    Techniques: Produced, Activation Assay