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Tocris pf 04418948
Effect of the EP3 receptor agonist sulprostone on the firing rate of LC neurons in the presence of the EP2 receptor antagonist <t>PF-04418948</t> or the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of sulprostone in the presence of PF-04418948 (10 µM) (A) or L-161,982 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C,D) Concentration-effect curves for sulprostone in control (filled squares) and in the presence of PF-04418948 (3 μM, open triangles or 10 μM, filled triangles) (C) or L-161,982 (3 μM, open diamonds or 10 μM, filled diamonds) (D) . The horizontal axes show the sulprostone concentration on a semi-logarithmic scale. The vertical axes express the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each sulprostone concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions.
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Inhibition of rat locus coeruleus neurons by prostaglandin E 2 EP3 receptors: pharmacological characterization ex vivo"

Article Title: Inhibition of rat locus coeruleus neurons by prostaglandin E 2 EP3 receptors: pharmacological characterization ex vivo

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2023.1290605

Effect of the EP3 receptor agonist sulprostone on the firing rate of LC neurons in the presence of the EP2 receptor antagonist PF-04418948 or the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of sulprostone in the presence of PF-04418948 (10 µM) (A) or L-161,982 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C,D) Concentration-effect curves for sulprostone in control (filled squares) and in the presence of PF-04418948 (3 μM, open triangles or 10 μM, filled triangles) (C) or L-161,982 (3 μM, open diamonds or 10 μM, filled diamonds) (D) . The horizontal axes show the sulprostone concentration on a semi-logarithmic scale. The vertical axes express the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each sulprostone concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions.
Figure Legend Snippet: Effect of the EP3 receptor agonist sulprostone on the firing rate of LC neurons in the presence of the EP2 receptor antagonist PF-04418948 or the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of sulprostone in the presence of PF-04418948 (10 µM) (A) or L-161,982 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C,D) Concentration-effect curves for sulprostone in control (filled squares) and in the presence of PF-04418948 (3 μM, open triangles or 10 μM, filled triangles) (C) or L-161,982 (3 μM, open diamonds or 10 μM, filled diamonds) (D) . The horizontal axes show the sulprostone concentration on a semi-logarithmic scale. The vertical axes express the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each sulprostone concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions.

Techniques Used: Concentration Assay, Construct

Effect of PGE 2 on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of PGE 2 in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for PGE 2 in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the PGE 2 concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each PGE 2 concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for PGE 2 is shifted to the right by the EP3 receptor antagonist and to the left by the EP2 and EP4 receptor antagonists.
Figure Legend Snippet: Effect of PGE 2 on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of PGE 2 in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for PGE 2 in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the PGE 2 concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each PGE 2 concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for PGE 2 is shifted to the right by the EP3 receptor antagonist and to the left by the EP2 and EP4 receptor antagonists.

Techniques Used: Concentration Assay, Construct

Effect of misoprostol on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of misoprostol in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for misoprostol in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the misoprostol concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each misoprostol concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for misoprostol is shifted to the right by the EP3 receptor antagonist.
Figure Legend Snippet: Effect of misoprostol on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of misoprostol in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for misoprostol in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the misoprostol concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each misoprostol concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for misoprostol is shifted to the right by the EP3 receptor antagonist.

Techniques Used: Concentration Assay, Construct


Structured Review

Tocris pf 04418948
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Structured Review

Tocris pf 04418948
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 04418948/product/Tocris
Average 86 stars, based on 1 article reviews
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pf 04418948 - by Bioz Stars, 2024-02
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Structured Review

Tocris pf 04418948
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 04418948/product/Tocris
Average 86 stars, based on 1 article reviews
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Structured Review

Tocris pf 04418948
a , Mice were infected intranasally with 25 μl of influenza A virus at low (10 5 EID 50 ml −1 ), medium (10 6 EID 50 ml −1 ) or high (10 7 EID 50 ml −1 ) dose and food intake, water intake, motility and body weight were subsequently monitored daily. EID 50 is the 50% egg infective dose. Data are mean ± s.e.m.; n = 6 mice per group. One-way ANOVA with Dunnett’s multiple comparison test compared with vehicle control. Food intake: P = 0.0048 (low), P < 0.0001 (medium), P < 0.0001 (high). Water intake: P = 0.8185 (low), P < 0.0001 (medium), P < 0.0001 (high). Motility: P = 0.5231 (low), P < 0.0001 (medium), P < 0.0001 (high). Body weight: P = 0.0002 (low), P < 0.0001 (medium), P < 0.0001 (high). Survival: P = 0.3173 (low), P = 0.0185 (medium), P = 0.0007 (high). b , Mice were infected with influenza A virus (all infections are with 10 6 EID 50 ml −1 unless otherwise indicated), given drinking water with or without 1 mg ml −1 ibuprofen, and monitored as indicated. Data are mean ± s.e.m.; n = 6 mice per group. Food intake: P < 0.0001; water intake: P = 0.0001; motility: P = 0.0001; body weight: P < 0.0001; survival: P = 0.0295. c , Mice were infected with influenza A virus, injected daily (intraperitoneal injection, 1 mg kg −1 ) with antagonists for EP1 (SC-51322), EP2 <t>(PF-04418948),</t> EP3 (DG-041) or EP4 (ONO-AE3-208), or vehicle alone, and monitored as indicated. Data are mean ± s.e.m.; n = 10 mice for vehicle groups; n = 8 mice for all others. For EP3 antagonist—food intake: P < 0.0001; water intake: P < 0.0001; motility: P < 0.0001; body weight: P = 0.0002; survival: P = 0.0094. b , c , Two-tailed unpaired t -test, with comparisons between groups treated with ibuprofen or EP3 antagonist and vehicle in c . Log-rank (Mantel–Cox) test for survival analyses; for behavioural or physiological changes, a mean daily change in behaviour (days 1–10 after infection or survival) was obtained for each mouse, and then used for comparisons across experimental groups (for more information see Extended Data Fig. ). * P < 0.05, ** P < 0.005, *** P <0.0005; NS, not significant.
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "An airway-to-brain sensory pathway mediates influenza-induced sickness"

Article Title: An airway-to-brain sensory pathway mediates influenza-induced sickness

Journal: Nature

doi: 10.1038/s41586-023-05796-0

a , Mice were infected intranasally with 25 μl of influenza A virus at low (10 5 EID 50 ml −1 ), medium (10 6 EID 50 ml −1 ) or high (10 7 EID 50 ml −1 ) dose and food intake, water intake, motility and body weight were subsequently monitored daily. EID 50 is the 50% egg infective dose. Data are mean ± s.e.m.; n = 6 mice per group. One-way ANOVA with Dunnett’s multiple comparison test compared with vehicle control. Food intake: P = 0.0048 (low), P < 0.0001 (medium), P < 0.0001 (high). Water intake: P = 0.8185 (low), P < 0.0001 (medium), P < 0.0001 (high). Motility: P = 0.5231 (low), P < 0.0001 (medium), P < 0.0001 (high). Body weight: P = 0.0002 (low), P < 0.0001 (medium), P < 0.0001 (high). Survival: P = 0.3173 (low), P = 0.0185 (medium), P = 0.0007 (high). b , Mice were infected with influenza A virus (all infections are with 10 6 EID 50 ml −1 unless otherwise indicated), given drinking water with or without 1 mg ml −1 ibuprofen, and monitored as indicated. Data are mean ± s.e.m.; n = 6 mice per group. Food intake: P < 0.0001; water intake: P = 0.0001; motility: P = 0.0001; body weight: P < 0.0001; survival: P = 0.0295. c , Mice were infected with influenza A virus, injected daily (intraperitoneal injection, 1 mg kg −1 ) with antagonists for EP1 (SC-51322), EP2 (PF-04418948), EP3 (DG-041) or EP4 (ONO-AE3-208), or vehicle alone, and monitored as indicated. Data are mean ± s.e.m.; n = 10 mice for vehicle groups; n = 8 mice for all others. For EP3 antagonist—food intake: P < 0.0001; water intake: P < 0.0001; motility: P < 0.0001; body weight: P = 0.0002; survival: P = 0.0094. b , c , Two-tailed unpaired t -test, with comparisons between groups treated with ibuprofen or EP3 antagonist and vehicle in c . Log-rank (Mantel–Cox) test for survival analyses; for behavioural or physiological changes, a mean daily change in behaviour (days 1–10 after infection or survival) was obtained for each mouse, and then used for comparisons across experimental groups (for more information see Extended Data Fig. ). * P < 0.05, ** P < 0.005, *** P <0.0005; NS, not significant.
Figure Legend Snippet: a , Mice were infected intranasally with 25 μl of influenza A virus at low (10 5 EID 50 ml −1 ), medium (10 6 EID 50 ml −1 ) or high (10 7 EID 50 ml −1 ) dose and food intake, water intake, motility and body weight were subsequently monitored daily. EID 50 is the 50% egg infective dose. Data are mean ± s.e.m.; n = 6 mice per group. One-way ANOVA with Dunnett’s multiple comparison test compared with vehicle control. Food intake: P = 0.0048 (low), P < 0.0001 (medium), P < 0.0001 (high). Water intake: P = 0.8185 (low), P < 0.0001 (medium), P < 0.0001 (high). Motility: P = 0.5231 (low), P < 0.0001 (medium), P < 0.0001 (high). Body weight: P = 0.0002 (low), P < 0.0001 (medium), P < 0.0001 (high). Survival: P = 0.3173 (low), P = 0.0185 (medium), P = 0.0007 (high). b , Mice were infected with influenza A virus (all infections are with 10 6 EID 50 ml −1 unless otherwise indicated), given drinking water with or without 1 mg ml −1 ibuprofen, and monitored as indicated. Data are mean ± s.e.m.; n = 6 mice per group. Food intake: P < 0.0001; water intake: P = 0.0001; motility: P = 0.0001; body weight: P < 0.0001; survival: P = 0.0295. c , Mice were infected with influenza A virus, injected daily (intraperitoneal injection, 1 mg kg −1 ) with antagonists for EP1 (SC-51322), EP2 (PF-04418948), EP3 (DG-041) or EP4 (ONO-AE3-208), or vehicle alone, and monitored as indicated. Data are mean ± s.e.m.; n = 10 mice for vehicle groups; n = 8 mice for all others. For EP3 antagonist—food intake: P < 0.0001; water intake: P < 0.0001; motility: P < 0.0001; body weight: P = 0.0002; survival: P = 0.0094. b , c , Two-tailed unpaired t -test, with comparisons between groups treated with ibuprofen or EP3 antagonist and vehicle in c . Log-rank (Mantel–Cox) test for survival analyses; for behavioural or physiological changes, a mean daily change in behaviour (days 1–10 after infection or survival) was obtained for each mouse, and then used for comparisons across experimental groups (for more information see Extended Data Fig. ). * P < 0.05, ** P < 0.005, *** P <0.0005; NS, not significant.

Techniques Used: Infection, Injection, Two Tailed Test


Structured Review

Tocris ep2
( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or <t>EP1/EP2</t> receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).
Ep2, supplied by Tocris, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice"

Article Title: A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice

Journal: eLife

doi: 10.7554/eLife.68205

( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or EP1/EP2 receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).
Figure Legend Snippet: ( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or EP1/EP2 receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).

Techniques Used: Injection, Infection

Statistical parameters for effects of dimethyl-PGE2 (dmPGE2), EP1 and  EP2  receptor blockers and CNO on gonadotropin-releasing hormone (GnRH)-green fluorescent protein (GFP) neuron firing rate ( <xref ref-type= Figure 4 ), p-values <0.05 are in bold font." title="... parameters for effects of dimethyl-PGE2 (dmPGE2), EP1 and EP2 receptor blockers and CNO on gonadotropin-releasing ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: Statistical parameters for effects of dimethyl-PGE2 (dmPGE2), EP1 and EP2 receptor blockers and CNO on gonadotropin-releasing hormone (GnRH)-green fluorescent protein (GFP) neuron firing rate ( Figure 4 ), p-values <0.05 are in bold font.

Techniques Used:


Structured Review

Tocris ep2 antagonist
Ep2 Antagonist, supplied by Tocris, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ep2 antagonist - by Bioz Stars, 2024-02
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Tocris pf
Pf, supplied by Tocris, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 92 stars, based on 1 article reviews
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pf - by Bioz Stars, 2024-02
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Tocris pf 04418948
Transient receptor potential ankyrin-1 (TRPA1)-mediated airway relaxation requires prostaglandins. The TRPA1 agonist allyl isothiocyanate (AITC; white circles) dose-dependently decreased bronchoconstriction caused by vagal nerve stimulation in guinea pigs in vivo. TRPA1-mediated airway relaxation was significantly inhibited by pretreatment with indomethacin in vivo (1 mg/kg; black circles; A) and in the organ bath [5 μM; AITC, white circles; AITC + indomethacin, black circles (B); cinnamaldehyde (CINN), white squares; CINN + indomethacin, black squares (C)]. TRPA1-mediated relaxation was also inhibited by the EP2 receptor antagonist <t>PF</t> <t>04418948</t> (30 μM; AITC, white circles; AITC + PF 04418948, black circles; D). Data represent means ± SD, n = 4 samples per group. *P < 0.01, **P < 0.001. Delta Ppi, change in peak pulmonary inflation pressure before and during vagal nerve stimulation; Max, maximum.
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 04418948/product/Tocris
Average 86 stars, based on 1 article reviews
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pf 04418948 - by Bioz Stars, 2024-02
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1) Product Images from "Transient receptor potential ankyrin-1 causes rapid bronchodilation via nonepithelial PGE 2"

Article Title: Transient receptor potential ankyrin-1 causes rapid bronchodilation via nonepithelial PGE 2

Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

doi: 10.1152/ajplung.00277.2019

Transient receptor potential ankyrin-1 (TRPA1)-mediated airway relaxation requires prostaglandins. The TRPA1 agonist allyl isothiocyanate (AITC; white circles) dose-dependently decreased bronchoconstriction caused by vagal nerve stimulation in guinea pigs in vivo. TRPA1-mediated airway relaxation was significantly inhibited by pretreatment with indomethacin in vivo (1 mg/kg; black circles; A) and in the organ bath [5 μM; AITC, white circles; AITC + indomethacin, black circles (B); cinnamaldehyde (CINN), white squares; CINN + indomethacin, black squares (C)]. TRPA1-mediated relaxation was also inhibited by the EP2 receptor antagonist PF 04418948 (30 μM; AITC, white circles; AITC + PF 04418948, black circles; D). Data represent means ± SD, n = 4 samples per group. *P < 0.01, **P < 0.001. Delta Ppi, change in peak pulmonary inflation pressure before and during vagal nerve stimulation; Max, maximum.
Figure Legend Snippet: Transient receptor potential ankyrin-1 (TRPA1)-mediated airway relaxation requires prostaglandins. The TRPA1 agonist allyl isothiocyanate (AITC; white circles) dose-dependently decreased bronchoconstriction caused by vagal nerve stimulation in guinea pigs in vivo. TRPA1-mediated airway relaxation was significantly inhibited by pretreatment with indomethacin in vivo (1 mg/kg; black circles; A) and in the organ bath [5 μM; AITC, white circles; AITC + indomethacin, black circles (B); cinnamaldehyde (CINN), white squares; CINN + indomethacin, black squares (C)]. TRPA1-mediated relaxation was also inhibited by the EP2 receptor antagonist PF 04418948 (30 μM; AITC, white circles; AITC + PF 04418948, black circles; D). Data represent means ± SD, n = 4 samples per group. *P < 0.01, **P < 0.001. Delta Ppi, change in peak pulmonary inflation pressure before and during vagal nerve stimulation; Max, maximum.

Techniques Used: In Vivo


Structured Review

Tocris pf 04418948
Transient receptor potential ankyrin-1 (TRPA1)-mediated airway relaxation requires prostaglandins. The TRPA1 agonist allyl isothiocyanate (AITC; white circles) dose-dependently decreased bronchoconstriction caused by vagal nerve stimulation in guinea pigs in vivo. TRPA1-mediated airway relaxation was significantly inhibited by pretreatment with indomethacin in vivo (1 mg/kg; black circles; A) and in the organ bath [5 μM; AITC, white circles; AITC + indomethacin, black circles (B); cinnamaldehyde (CINN), white squares; CINN + indomethacin, black squares (C)]. TRPA1-mediated relaxation was also inhibited by the EP2 receptor antagonist <t>PF</t> <t>04418948</t> (30 μM; AITC, white circles; AITC + PF 04418948, black circles; D). Data represent means ± SD, n = 4 samples per group. *P < 0.01, **P < 0.001. Delta Ppi, change in peak pulmonary inflation pressure before and during vagal nerve stimulation; Max, maximum.
Pf 04418948, supplied by Tocris, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pf 04418948/product/Tocris
Average 92 stars, based on 1 article reviews
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92/100 stars

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1) Product Images from "Transient receptor potential ankyrin-1 causes rapid bronchodilation via nonepithelial PGE 2"

Article Title: Transient receptor potential ankyrin-1 causes rapid bronchodilation via nonepithelial PGE 2

Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

doi: 10.1152/ajplung.00277.2019

Transient receptor potential ankyrin-1 (TRPA1)-mediated airway relaxation requires prostaglandins. The TRPA1 agonist allyl isothiocyanate (AITC; white circles) dose-dependently decreased bronchoconstriction caused by vagal nerve stimulation in guinea pigs in vivo. TRPA1-mediated airway relaxation was significantly inhibited by pretreatment with indomethacin in vivo (1 mg/kg; black circles; A) and in the organ bath [5 μM; AITC, white circles; AITC + indomethacin, black circles (B); cinnamaldehyde (CINN), white squares; CINN + indomethacin, black squares (C)]. TRPA1-mediated relaxation was also inhibited by the EP2 receptor antagonist PF 04418948 (30 μM; AITC, white circles; AITC + PF 04418948, black circles; D). Data represent means ± SD, n = 4 samples per group. *P < 0.01, **P < 0.001. Delta Ppi, change in peak pulmonary inflation pressure before and during vagal nerve stimulation; Max, maximum.
Figure Legend Snippet: Transient receptor potential ankyrin-1 (TRPA1)-mediated airway relaxation requires prostaglandins. The TRPA1 agonist allyl isothiocyanate (AITC; white circles) dose-dependently decreased bronchoconstriction caused by vagal nerve stimulation in guinea pigs in vivo. TRPA1-mediated airway relaxation was significantly inhibited by pretreatment with indomethacin in vivo (1 mg/kg; black circles; A) and in the organ bath [5 μM; AITC, white circles; AITC + indomethacin, black circles (B); cinnamaldehyde (CINN), white squares; CINN + indomethacin, black squares (C)]. TRPA1-mediated relaxation was also inhibited by the EP2 receptor antagonist PF 04418948 (30 μM; AITC, white circles; AITC + PF 04418948, black circles; D). Data represent means ± SD, n = 4 samples per group. *P < 0.01, **P < 0.001. Delta Ppi, change in peak pulmonary inflation pressure before and during vagal nerve stimulation; Max, maximum.

Techniques Used: In Vivo

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    Tocris pf 04418948
    Effect of the EP3 receptor agonist sulprostone on the firing rate of LC neurons in the presence of the EP2 receptor antagonist <t>PF-04418948</t> or the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of sulprostone in the presence of PF-04418948 (10 µM) (A) or L-161,982 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C,D) Concentration-effect curves for sulprostone in control (filled squares) and in the presence of PF-04418948 (3 μM, open triangles or 10 μM, filled triangles) (C) or L-161,982 (3 μM, open diamonds or 10 μM, filled diamonds) (D) . The horizontal axes show the sulprostone concentration on a semi-logarithmic scale. The vertical axes express the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each sulprostone concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions.
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    ep2  (Tocris)
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    ( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or <t>EP1/EP2</t> receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).
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    ( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or <t>EP1/EP2</t> receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).
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    ( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or <t>EP1/EP2</t> receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).
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    Effect of the EP3 receptor agonist sulprostone on the firing rate of LC neurons in the presence of the EP2 receptor antagonist PF-04418948 or the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of sulprostone in the presence of PF-04418948 (10 µM) (A) or L-161,982 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C,D) Concentration-effect curves for sulprostone in control (filled squares) and in the presence of PF-04418948 (3 μM, open triangles or 10 μM, filled triangles) (C) or L-161,982 (3 μM, open diamonds or 10 μM, filled diamonds) (D) . The horizontal axes show the sulprostone concentration on a semi-logarithmic scale. The vertical axes express the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each sulprostone concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions.

    Journal: Frontiers in Pharmacology

    Article Title: Inhibition of rat locus coeruleus neurons by prostaglandin E 2 EP3 receptors: pharmacological characterization ex vivo

    doi: 10.3389/fphar.2023.1290605

    Figure Lengend Snippet: Effect of the EP3 receptor agonist sulprostone on the firing rate of LC neurons in the presence of the EP2 receptor antagonist PF-04418948 or the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of sulprostone in the presence of PF-04418948 (10 µM) (A) or L-161,982 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C,D) Concentration-effect curves for sulprostone in control (filled squares) and in the presence of PF-04418948 (3 μM, open triangles or 10 μM, filled triangles) (C) or L-161,982 (3 μM, open diamonds or 10 μM, filled diamonds) (D) . The horizontal axes show the sulprostone concentration on a semi-logarithmic scale. The vertical axes express the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each sulprostone concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions.

    Article Snippet: For electrophysiological recordings, the following drugs were used (drug source): BaCl 2 (Sigma-Aldrich Química S.A., Madrid, Spain), γ-aminobutyric acid (GABA, Sigma-Aldrich), L-161,982 (Tocris Bioscience, Bristol, UK), L-798,106 (Tocris Bioscience), [Met]enkephaline acetate salt (Bachem, Weil am Rhein, Germany), misoprostol free acid (Cayman Chemical, Ann Arbor, MI, USA), pertussis toxin (Tocris Bioscience), PF-04418948 (Tocris Bioscience), prostaglandin E 2 (PGE 2 ) (Tocris Bioscience), SCH-23390 (Tocris Bioscience) and sulprostone (Cayman Chemical).

    Techniques: Concentration Assay, Construct

    Effect of PGE 2 on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of PGE 2 in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for PGE 2 in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the PGE 2 concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each PGE 2 concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for PGE 2 is shifted to the right by the EP3 receptor antagonist and to the left by the EP2 and EP4 receptor antagonists.

    Journal: Frontiers in Pharmacology

    Article Title: Inhibition of rat locus coeruleus neurons by prostaglandin E 2 EP3 receptors: pharmacological characterization ex vivo

    doi: 10.3389/fphar.2023.1290605

    Figure Lengend Snippet: Effect of PGE 2 on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of PGE 2 in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for PGE 2 in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the PGE 2 concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each PGE 2 concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for PGE 2 is shifted to the right by the EP3 receptor antagonist and to the left by the EP2 and EP4 receptor antagonists.

    Article Snippet: For electrophysiological recordings, the following drugs were used (drug source): BaCl 2 (Sigma-Aldrich Química S.A., Madrid, Spain), γ-aminobutyric acid (GABA, Sigma-Aldrich), L-161,982 (Tocris Bioscience, Bristol, UK), L-798,106 (Tocris Bioscience), [Met]enkephaline acetate salt (Bachem, Weil am Rhein, Germany), misoprostol free acid (Cayman Chemical, Ann Arbor, MI, USA), pertussis toxin (Tocris Bioscience), PF-04418948 (Tocris Bioscience), prostaglandin E 2 (PGE 2 ) (Tocris Bioscience), SCH-23390 (Tocris Bioscience) and sulprostone (Cayman Chemical).

    Techniques: Concentration Assay, Construct

    Effect of misoprostol on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of misoprostol in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for misoprostol in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the misoprostol concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each misoprostol concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for misoprostol is shifted to the right by the EP3 receptor antagonist.

    Journal: Frontiers in Pharmacology

    Article Title: Inhibition of rat locus coeruleus neurons by prostaglandin E 2 EP3 receptors: pharmacological characterization ex vivo

    doi: 10.3389/fphar.2023.1290605

    Figure Lengend Snippet: Effect of misoprostol on the firing rate of LC neurons in the absence or presence of the EP3 receptor antagonist L-798,106 or a combination of the EP2 receptor antagonist PF-04418948 and the EP4 receptor antagonist L-161,982. (A,B) Representative examples of firing rate recordings of two LC neurons showing the effect of increasing concentrations of misoprostol in the absence (A) and presence of L-798,106 (10 µM) (B) . The vertical lines represent the number of spikes recorded every 10 s and the horizontal bars the period of drug application. (C) Concentration-effect curves for misoprostol in control (filled squares) and in the presence of L-798,106 (10 μM, filled circles) or PF-04418948 and L-161,982 (10 µM each, half-filled diamonds). The horizontal axis shows the misoprostol concentration on a semi-logarithmic scale. The vertical axis expresses the reduction in firing rate of LC neurons as the percentage of the baseline. Data points are the mean ± SEM at each misoprostol concentration obtained from n number of experiments. The lines through the data are the theoretical curves in each group constructed from the mean of the individual concentration-effect curve parameters, as estimated by nonlinear regressions. Note that the concentration-effect curve for misoprostol is shifted to the right by the EP3 receptor antagonist.

    Article Snippet: For electrophysiological recordings, the following drugs were used (drug source): BaCl 2 (Sigma-Aldrich Química S.A., Madrid, Spain), γ-aminobutyric acid (GABA, Sigma-Aldrich), L-161,982 (Tocris Bioscience, Bristol, UK), L-798,106 (Tocris Bioscience), [Met]enkephaline acetate salt (Bachem, Weil am Rhein, Germany), misoprostol free acid (Cayman Chemical, Ann Arbor, MI, USA), pertussis toxin (Tocris Bioscience), PF-04418948 (Tocris Bioscience), prostaglandin E 2 (PGE 2 ) (Tocris Bioscience), SCH-23390 (Tocris Bioscience) and sulprostone (Cayman Chemical).

    Techniques: Concentration Assay, Construct

    ( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or EP1/EP2 receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).

    Journal: eLife

    Article Title: A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice

    doi: 10.7554/eLife.68205

    Figure Lengend Snippet: ( A,B ) Representative examples of GnRH neuron firing rate response to dmPGE2 following vehicle pretreatment ( A ) or EP1/EP2 receptor antagonists ( B ). ( C ) Left, mean firing of individual neurons in each period; right, group mean ± SEM, *p<0.05, **p<0.0001, two-way repeated-measure ANOVA/Bonferroni (vehicle n=9 from five mice, EP1/EP2 antag n=10 from five mice). ( D ) Representative example of Tac2-GFP neuron response to dmPGE2. Note Y-axis is zoomed in compared to A-C. ( E ) Left, mean firing of individual neurons in each period; right, group mean ± SEM (n=9). ( F,G ) Representative examples of GnRH neurons from mice injected with AAV-Gq in the POA in which pretreatment with EP1/EP2 receptor antagonists blocked ( F ) or reduced response ( G ) to CNO. ( H ) Left, mean firing of individual neurons in each period, the single magenta line shows a cell in a slice with AAV-Dq infected neurons (n=12 from seven mice), which was omitted from the group mean ± SEM on the right (n=11 from seven mice).

    Article Snippet: Antagonists for prostaglandin receptor EP1 (SC-19220, 100 μM, Tocris) and EP2 (PF-04418948, 20 μM, Tocris) were diluted into fresh bubbled ACSF (final DMSO concentration 0.3%) and bath applied before CNO treatment.

    Techniques: Injection, Infection

    Statistical parameters for effects of dimethyl-PGE2 (dmPGE2), EP1 and  EP2  receptor blockers and CNO on gonadotropin-releasing hormone (GnRH)-green fluorescent protein (GFP) neuron firing rate ( <xref ref-type= Figure 4 ), p-values <0.05 are in bold font." width="100%" height="100%">

    Journal: eLife

    Article Title: A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice

    doi: 10.7554/eLife.68205

    Figure Lengend Snippet: Statistical parameters for effects of dimethyl-PGE2 (dmPGE2), EP1 and EP2 receptor blockers and CNO on gonadotropin-releasing hormone (GnRH)-green fluorescent protein (GFP) neuron firing rate ( Figure 4 ), p-values <0.05 are in bold font.

    Article Snippet: Antagonists for prostaglandin receptor EP1 (SC-19220, 100 μM, Tocris) and EP2 (PF-04418948, 20 μM, Tocris) were diluted into fresh bubbled ACSF (final DMSO concentration 0.3%) and bath applied before CNO treatment.

    Techniques: