am404  (Alomone Labs)


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    Structured Review

    Alomone Labs am404
    Effects of intracerebral <t>AM404</t> on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P
    Am404, 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
    https://www.bioz.com/result/am404/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    am404 - by Bioz Stars, 2021-12
    94/100 stars

    Images

    1) Product Images from "Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia"

    Article Title: Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia

    Journal: JCI Insight

    doi: 10.1172/jci.insight.145632

    Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P
    Figure Legend Snippet: Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P

    Techniques Used: Injection

    Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P
    Figure Legend Snippet: Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P

    Techniques Used: Injection, Mouse Assay

    2) Product Images from "Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia"

    Article Title: Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia

    Journal: JCI Insight

    doi: 10.1172/jci.insight.145632

    Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P
    Figure Legend Snippet: Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P

    Techniques Used: Injection

    Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P
    Figure Legend Snippet: Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P

    Techniques Used: Injection, Mouse Assay

    3) Product Images from "Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia"

    Article Title: Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia

    Journal: JCI Insight

    doi: 10.1172/jci.insight.145632

    Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P
    Figure Legend Snippet: Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P

    Techniques Used: Injection

    Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P
    Figure Legend Snippet: Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P

    Techniques Used: Injection, Mouse Assay

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    Alomone Labs kt5720
    PKA activity is required after memory retrieval at 6 but not 24 h after training for later memory expression. Six hours ( A ) or 24 h ( B ) after a single CS/US pairing (0 h), animals received a CS stimulation or no stimulation (no CS), followed 10 min later by an injection with either a PKA inhibitor <t>(KT5720)</t> or vehicle. In each group, baseline levels are defined by the mean feeding response level to the CS (line) ± SEM (gray band) of a group of animals handled in parallel ( n = 17). A , ANOVAs followed by pairwise post hoc tests reveal that the two groups ( n = 24 and 21) first tested at 6 h after training and 10 min before injection show significantly (*) elevated feeding responses to the CS compared with baseline level. At the second test, 24 h after training, one-way ANOVAs detected a source of significant difference. Of the four CS/US paired groups, only the group that received the CS at 6 h after training followed by KT5720 injection shows a feeding response to the CS that does not differ from baseline. A two-way ANOVA comparing the feeding responses to the CS of the four CS/US paired groups at 24 h detected a significant interaction of memory retrieval at 6 h and subsequent PKA inhibition. B , The two groups ( n = 17 and 20) first tested at 24 h after training and 10 min before injection show significantly (*) elevated feeding responses to the CS compared with the baseline level. At 42 h after training, one-way ANOVAs and multiple post hoc ).
    Kt5720, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kt5720/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kt5720 - by Bioz Stars, 2021-12
    91/100 stars
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    94
    Alomone Labs drugs am404
    Effects of <t>AM404</t> on [ 3 H]D-Asp release in hippocampal synaptosomes and intracellular Ca 2+ responses. (A) Time course of [ 3 H]D-Asp release induced by NMDA plus Gly and effects of AM404 in hippocampal synaptosomes. Results are expressed as fractional rate percent. (B) AM404 inhibition of the NMDA plus Glycine-evoked-[ 3 H]D-Asp release in hippocampal synaptosomes. (C) Data of calcium imaging expressed as fluorescence intensity (ΔF/F baseline) vs. time. (D) Data of calcium imaging calculated the area under the curve (AUC). Data are means ± SEM of three independent experiments. # p
    Drugs Am404, 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
    https://www.bioz.com/result/drugs am404/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    drugs am404 - by Bioz Stars, 2021-12
    94/100 stars
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    PKA activity is required after memory retrieval at 6 but not 24 h after training for later memory expression. Six hours ( A ) or 24 h ( B ) after a single CS/US pairing (0 h), animals received a CS stimulation or no stimulation (no CS), followed 10 min later by an injection with either a PKA inhibitor (KT5720) or vehicle. In each group, baseline levels are defined by the mean feeding response level to the CS (line) ± SEM (gray band) of a group of animals handled in parallel ( n = 17). A , ANOVAs followed by pairwise post hoc tests reveal that the two groups ( n = 24 and 21) first tested at 6 h after training and 10 min before injection show significantly (*) elevated feeding responses to the CS compared with baseline level. At the second test, 24 h after training, one-way ANOVAs detected a source of significant difference. Of the four CS/US paired groups, only the group that received the CS at 6 h after training followed by KT5720 injection shows a feeding response to the CS that does not differ from baseline. A two-way ANOVA comparing the feeding responses to the CS of the four CS/US paired groups at 24 h detected a significant interaction of memory retrieval at 6 h and subsequent PKA inhibition. B , The two groups ( n = 17 and 20) first tested at 24 h after training and 10 min before injection show significantly (*) elevated feeding responses to the CS compared with the baseline level. At 42 h after training, one-way ANOVAs and multiple post hoc ).

    Journal: The Journal of Neuroscience

    Article Title: Phase-Dependent Molecular Requirements for Memory Reconsolidation: Differential Roles for Protein Synthesis and Protein Kinase A Activity

    doi: 10.1523/JNEUROSCI.0890-06.2006

    Figure Lengend Snippet: PKA activity is required after memory retrieval at 6 but not 24 h after training for later memory expression. Six hours ( A ) or 24 h ( B ) after a single CS/US pairing (0 h), animals received a CS stimulation or no stimulation (no CS), followed 10 min later by an injection with either a PKA inhibitor (KT5720) or vehicle. In each group, baseline levels are defined by the mean feeding response level to the CS (line) ± SEM (gray band) of a group of animals handled in parallel ( n = 17). A , ANOVAs followed by pairwise post hoc tests reveal that the two groups ( n = 24 and 21) first tested at 6 h after training and 10 min before injection show significantly (*) elevated feeding responses to the CS compared with baseline level. At the second test, 24 h after training, one-way ANOVAs detected a source of significant difference. Of the four CS/US paired groups, only the group that received the CS at 6 h after training followed by KT5720 injection shows a feeding response to the CS that does not differ from baseline. A two-way ANOVA comparing the feeding responses to the CS of the four CS/US paired groups at 24 h detected a significant interaction of memory retrieval at 6 h and subsequent PKA inhibition. B , The two groups ( n = 17 and 20) first tested at 24 h after training and 10 min before injection show significantly (*) elevated feeding responses to the CS compared with the baseline level. At 42 h after training, one-way ANOVAs and multiple post hoc ).

    Article Snippet: The amnestic agent used was KT5720 (Alomone Labs, Jerusalem, Israel), a specific PKA inhibitor, at 10 μ m in 0.5% DMSO (final concentrations), whereas the vehicle was a mixture of saline and 0.5% DMSO.

    Techniques: Activity Assay, Expressing, Injection, Inhibition

    A conserved functional PKA catalytic subunit (PKA C) is present in the Lymnaea CNS. ( A ) cAMP stimulates PKA C activity in Lymnaea nervous system extracts ( Ai ) and purified PKA fractions ( Aii ), which can be blocked by KT5720 or PKAI. The whole CNS data (mean ±SEM) come from experiments with single brains ( n = 19). *, P

    Journal: Learning & Memory

    Article Title: Different phases of long-term memory require distinct temporal patterns of PKA activity after single-trial classical conditioning

    doi: 10.1101/lm.1088408

    Figure Lengend Snippet: A conserved functional PKA catalytic subunit (PKA C) is present in the Lymnaea CNS. ( A ) cAMP stimulates PKA C activity in Lymnaea nervous system extracts ( Ai ) and purified PKA fractions ( Aii ), which can be blocked by KT5720 or PKAI. The whole CNS data (mean ±SEM) come from experiments with single brains ( n = 19). *, P

    Article Snippet: Snails from one of the KT5720 and vehicle-injected groups each were tested at 6 h while the remaining KT5720 and vehicle-injected snails were tested at 24 h post-training for their feeding responses to the CS.

    Techniques: Functional Assay, Activity Assay, Purification

    Effects of AM404 on [ 3 H]D-Asp release in hippocampal synaptosomes and intracellular Ca 2+ responses. (A) Time course of [ 3 H]D-Asp release induced by NMDA plus Gly and effects of AM404 in hippocampal synaptosomes. Results are expressed as fractional rate percent. (B) AM404 inhibition of the NMDA plus Glycine-evoked-[ 3 H]D-Asp release in hippocampal synaptosomes. (C) Data of calcium imaging expressed as fluorescence intensity (ΔF/F baseline) vs. time. (D) Data of calcium imaging calculated the area under the curve (AUC). Data are means ± SEM of three independent experiments. # p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Neuroprotective Effect of AM404 Against NMDA-Induced Hippocampal Excitotoxicity

    doi: 10.3389/fncel.2019.00566

    Figure Lengend Snippet: Effects of AM404 on [ 3 H]D-Asp release in hippocampal synaptosomes and intracellular Ca 2+ responses. (A) Time course of [ 3 H]D-Asp release induced by NMDA plus Gly and effects of AM404 in hippocampal synaptosomes. Results are expressed as fractional rate percent. (B) AM404 inhibition of the NMDA plus Glycine-evoked-[ 3 H]D-Asp release in hippocampal synaptosomes. (C) Data of calcium imaging expressed as fluorescence intensity (ΔF/F baseline) vs. time. (D) Data of calcium imaging calculated the area under the curve (AUC). Data are means ± SEM of three independent experiments. # p

    Article Snippet: Drugs AM404 (Alomone Labs) was dissolved in the physiological medium for the synaptosome experiment and in DMSO for the other experiments (Merck KGaA, Darmstadt, Germany).

    Techniques: Inhibition, Imaging, Fluorescence

    Effects of AM404 on NMDA-induced inflammatory mediators in organotypic hippocampal slices cultures (OHSC). OHSCs were pre-treated with two concentrations of AM404 (25 or 50 μM) for 30 min before stimulating with 10 ng/ml LPS or 25 μM NMDA. After 4 h, interleukin (IL)-1β (A) , IL-6 (B) , TNFα (C) , mPGES-1 (D) , and iNOS (E) were measured by PCR. After 24 h, COX-2 (F) was evaluated by western blot (WB). Data are expressed as mean ± SEM of at least three OHSCs/group. * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Neuroprotective Effect of AM404 Against NMDA-Induced Hippocampal Excitotoxicity

    doi: 10.3389/fncel.2019.00566

    Figure Lengend Snippet: Effects of AM404 on NMDA-induced inflammatory mediators in organotypic hippocampal slices cultures (OHSC). OHSCs were pre-treated with two concentrations of AM404 (25 or 50 μM) for 30 min before stimulating with 10 ng/ml LPS or 25 μM NMDA. After 4 h, interleukin (IL)-1β (A) , IL-6 (B) , TNFα (C) , mPGES-1 (D) , and iNOS (E) were measured by PCR. After 24 h, COX-2 (F) was evaluated by western blot (WB). Data are expressed as mean ± SEM of at least three OHSCs/group. * p

    Article Snippet: Drugs AM404 (Alomone Labs) was dissolved in the physiological medium for the synaptosome experiment and in DMSO for the other experiments (Merck KGaA, Darmstadt, Germany).

    Techniques: Polymerase Chain Reaction, Western Blot

    Effect of AM404 on microglia and astrocyte after 25 μM NMDA in OHSC. The OHSCs were pre-treated with two concentrations of AM404 (25 or 50 μM) for 30 min before stimulating with 25 μM NMDA. After 4 h, microglia markers, Iba-1 (A) , CSF1R (B) and CD11b (C) , an astrocyte marker, GFAP (D) were measured by qPCR. Data are expressed as mean ± SEM of at least three OHSCs/group. * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Neuroprotective Effect of AM404 Against NMDA-Induced Hippocampal Excitotoxicity

    doi: 10.3389/fncel.2019.00566

    Figure Lengend Snippet: Effect of AM404 on microglia and astrocyte after 25 μM NMDA in OHSC. The OHSCs were pre-treated with two concentrations of AM404 (25 or 50 μM) for 30 min before stimulating with 25 μM NMDA. After 4 h, microglia markers, Iba-1 (A) , CSF1R (B) and CD11b (C) , an astrocyte marker, GFAP (D) were measured by qPCR. Data are expressed as mean ± SEM of at least three OHSCs/group. * p

    Article Snippet: Drugs AM404 (Alomone Labs) was dissolved in the physiological medium for the synaptosome experiment and in DMSO for the other experiments (Merck KGaA, Darmstadt, Germany).

    Techniques: Marker, Real-time Polymerase Chain Reaction

    Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P

    Journal: JCI Insight

    Article Title: Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia

    doi: 10.1172/jci.insight.145632

    Figure Lengend Snippet: Effects of intracerebral AM404 on haloperidol-induced VCMs in rodents. ( A ) Rats ( n = 5–7 per group) were treated daily with oral haloperidol (1 mg/kg/d) for 21 days and received AM404 (0, 10, or 50 nmol) via intracerebroventricular injection at 23 hours after the last administration of haloperidol. The number of VCMs was measured for 3 minutes starting 30 minutes after the administration of AM404. After the experiment, the injection sites were confirmed by injecting Evans blue through the same cannula. A representative image of consecutive coronal sections is shown (43 mm wide in actual size). Individual data are shown with the mean ± SEM. Statistical significance was tested using 1-way ANOVA with post hoc Tukey’s test. * P

    Article Snippet: Haloperidol was purchased from Tokyo Chemical Industry; acetaminophen and capsaicin from Nacalai Tesque; AM404 from Alomone Labs; methamphetamine from Sumitomo Dainippon Pharma; CNO from Cayman Chemical; DL-2-amino-5-phosphonopentanoic acid (DL-APV) from MilliporeSigma; dinitroquinoxaline-2,3(1H,4H)-dione (DNQX) from Tocris Bioscience (Bio-Techne); bicuculline from Enzo Life Science; and pentobarbital from Kyoritsu Seiyaku.

    Techniques: Injection

    Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P

    Journal: JCI Insight

    Article Title: Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia

    doi: 10.1172/jci.insight.145632

    Figure Lengend Snippet: Effects of the dorsal striatal injection of AM404 and capsaicin on haloperidol-induced VCMs in WT and TRPV1-KO mice. WT and TRPV1-KO mice were treated daily with orally administrated haloperidol (2 mg/kg/d) for 21 days. On day 22, after VCMs were counted for 5 minutes as an initial baseline, half of the mice received vehicle (group 1), and the rest received AM404 (1 pmol/side) or capsaicin (10 ng/side) (group 2) through a preimplanted cannula in the dorsal striatum. Five minutes later, the number of VCMs was counted for another 5 minutes to determine the effect of the injected drug. The daily haloperidol treatment was continued for 4 more days; on day 26, the second set of VCM measurements was performed in a crossover design, with AM404 or capsaicin injection in group 1 and vehicle injection in group 2. ( A and B ) Effects of the dorsal striatal injection of AM404 on haloperidol-induced VCMs ( n = 9 per group). ( C and D ) Effects of the dorsal striatal injection of capsaicin on haloperidol-induced VCMs ( n = 7 per group). Changes in the number of VCMs are represented for individual mice on days 22 and 26 as percentages of the baseline VCM count. Open and filled circles indicate the results from groups 1 and 2, respectively. Statistical significance was tested using repeated measures 2-way ANOVA with post hoc multiple comparisons; * P

    Article Snippet: Haloperidol was purchased from Tokyo Chemical Industry; acetaminophen and capsaicin from Nacalai Tesque; AM404 from Alomone Labs; methamphetamine from Sumitomo Dainippon Pharma; CNO from Cayman Chemical; DL-2-amino-5-phosphonopentanoic acid (DL-APV) from MilliporeSigma; dinitroquinoxaline-2,3(1H,4H)-dione (DNQX) from Tocris Bioscience (Bio-Techne); bicuculline from Enzo Life Science; and pentobarbital from Kyoritsu Seiyaku.

    Techniques: Injection, Mouse Assay