sq 22536 Search Results


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Biosynth Carbosynth tetrahydro 29 furyl adenine sq 22536
Figure 11. IP3-gated stores and phospholipase C contribute to the cannabinoid enhancement of the NMDA-evoked Ca 21 signal. A, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the IP3 receptor antagonist xestospongin C (1 mM) or the vehicle control (DMSO). Xestospongin C dramatically reduced the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Results are from a single culture set; similar results were obtained in an additional three culture sets. B, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phospholipase C inhibitor U73122 (2 mM) or its inactive analog U-73343 (2 mM). The R(1)-WIN enhancement of the NMDA-evoked Ca 21 signal was blocked by U-73122. Results are from a single culture set; similar results were obtained in an additional two culture sets. C, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phosphodiesterase inhibitor IBMX (200 mM) or the adenylyl cyclase inhibitor SQ <t>22536</t> (200 mM). Neither agent blocked the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Each set of results is from a single culture set; similar results were obtained in an additional four culture sets for IBMX and two culture sets for SQ 22536. Numbers in the bars represent the number of neurons measured for each condition. *Significant difference from the respective control condition ( p , 0.05, Mann–Whitney U test).
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Figure 11. IP3-gated stores and phospholipase C contribute to the cannabinoid enhancement of the NMDA-evoked Ca 21 signal. A, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the IP3 receptor antagonist xestospongin C (1 mM) or the vehicle control (DMSO). Xestospongin C dramatically reduced the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Results are from a single culture set; similar results were obtained in an additional three culture sets. B, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phospholipase C inhibitor U73122 (2 mM) or its inactive analog U-73343 (2 mM). The R(1)-WIN enhancement of the NMDA-evoked Ca 21 signal was blocked by U-73122. Results are from a single culture set; similar results were obtained in an additional two culture sets. C, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phosphodiesterase inhibitor IBMX (200 mM) or the adenylyl cyclase inhibitor SQ <t>22536</t> (200 mM). Neither agent blocked the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Each set of results is from a single culture set; similar results were obtained in an additional four culture sets for IBMX and two culture sets for SQ 22536. Numbers in the bars represent the number of neurons measured for each condition. *Significant difference from the respective control condition ( p , 0.05, Mann–Whitney U test).
Sq 22536, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Figure 11. IP3-gated stores and phospholipase C contribute to the cannabinoid enhancement of the NMDA-evoked Ca 21 signal. A, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the IP3 receptor antagonist xestospongin C (1 mM) or the vehicle control (DMSO). Xestospongin C dramatically reduced the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Results are from a single culture set; similar results were obtained in an additional three culture sets. B, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phospholipase C inhibitor U73122 (2 mM) or its inactive analog U-73343 (2 mM). The R(1)-WIN enhancement of the NMDA-evoked Ca 21 signal was blocked by U-73122. Results are from a single culture set; similar results were obtained in an additional two culture sets. C, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phosphodiesterase inhibitor IBMX (200 mM) or the adenylyl cyclase inhibitor SQ <t>22536</t> (200 mM). Neither agent blocked the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Each set of results is from a single culture set; similar results were obtained in an additional four culture sets for IBMX and two culture sets for SQ 22536. Numbers in the bars represent the number of neurons measured for each condition. *Significant difference from the respective control condition ( p , 0.05, Mann–Whitney U test).
Adenylyl Cyclase Inhibitor Sq 22536, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ICN Pharmaceuticals 9-(tetrahydro-2-furanyl)-9h-purin-6-amine (sq 22536)
Figure 11. IP3-gated stores and phospholipase C contribute to the cannabinoid enhancement of the NMDA-evoked Ca 21 signal. A, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the IP3 receptor antagonist xestospongin C (1 mM) or the vehicle control (DMSO). Xestospongin C dramatically reduced the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Results are from a single culture set; similar results were obtained in an additional three culture sets. B, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phospholipase C inhibitor U73122 (2 mM) or its inactive analog U-73343 (2 mM). The R(1)-WIN enhancement of the NMDA-evoked Ca 21 signal was blocked by U-73122. Results are from a single culture set; similar results were obtained in an additional two culture sets. C, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phosphodiesterase inhibitor IBMX (200 mM) or the adenylyl cyclase inhibitor SQ <t>22536</t> (200 mM). Neither agent blocked the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Each set of results is from a single culture set; similar results were obtained in an additional four culture sets for IBMX and two culture sets for SQ 22536. Numbers in the bars represent the number of neurons measured for each condition. *Significant difference from the respective control condition ( p , 0.05, Mann–Whitney U test).
9 (Tetrahydro 2 Furanyl) 9h Purin 6 Amine (Sq 22536), supplied by ICN Pharmaceuticals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Figure 11. IP3-gated stores and phospholipase C contribute to the cannabinoid enhancement of the NMDA-evoked Ca 21 signal. A, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the IP3 receptor antagonist xestospongin C (1 mM) or the vehicle control (DMSO). Xestospongin C dramatically reduced the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Results are from a single culture set; similar results were obtained in an additional three culture sets. B, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phospholipase C inhibitor U73122 (2 mM) or its inactive analog U-73343 (2 mM). The R(1)-WIN enhancement of the NMDA-evoked Ca 21 signal was blocked by U-73122. Results are from a single culture set; similar results were obtained in an additional two culture sets. C, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phosphodiesterase inhibitor IBMX (200 mM) or the adenylyl cyclase inhibitor SQ 22536 (200 mM). Neither agent blocked the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Each set of results is from a single culture set; similar results were obtained in an additional four culture sets for IBMX and two culture sets for SQ 22536. Numbers in the bars represent the number of neurons measured for each condition. *Significant difference from the respective control condition ( p , 0.05, Mann–Whitney U test).

Journal: The Journal of Neuroscience

Article Title: Cannabinoids Enhance NMDA-Elicited Ca2+Signals in Cerebellar Granule Neurons in Culture

doi: 10.1523/jneurosci.19-20-08765.1999

Figure Lengend Snippet: Figure 11. IP3-gated stores and phospholipase C contribute to the cannabinoid enhancement of the NMDA-evoked Ca 21 signal. A, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the IP3 receptor antagonist xestospongin C (1 mM) or the vehicle control (DMSO). Xestospongin C dramatically reduced the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Results are from a single culture set; similar results were obtained in an additional three culture sets. B, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phospholipase C inhibitor U73122 (2 mM) or its inactive analog U-73343 (2 mM). The R(1)-WIN enhancement of the NMDA-evoked Ca 21 signal was blocked by U-73122. Results are from a single culture set; similar results were obtained in an additional two culture sets. C, Mean 6 SEM peak amplitude of the Ca 21 signals elicited by NMDA before and after application of 10 nM R(1)-WIN in cultures treated with the phosphodiesterase inhibitor IBMX (200 mM) or the adenylyl cyclase inhibitor SQ 22536 (200 mM). Neither agent blocked the R(1)-WIN enhancement of the Ca 21 signal to NMDA. Each set of results is from a single culture set; similar results were obtained in an additional four culture sets for IBMX and two culture sets for SQ 22536. Numbers in the bars represent the number of neurons measured for each condition. *Significant difference from the respective control condition ( p , 0.05, Mann–Whitney U test).

Article Snippet: Additional chemicals were purchased from the following companies: fura-2 AM, pluronic F-127, and thapsigargin from Molecular Probes; [3-(1,1-dimethylheptyl)-(2)-11-hydroxy-delta-8-tetrahydrocannabinol] (HU-210), 6-nitro-7-sulfamoylbenzo[f]quinoxaline-2,3-dione (NBQX), ( S)-a-methyl-4-carboxyphenylglycine (MC PG), D-(2)-2-amino-5phosphonopentanoic acid (D-AP5), and verapamil from Tocris Neuramin (Ballwin, MO); R(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate [R(1)-WIN] and S(2)-[2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate [S(2)-WIN] from Research Biochemicals (RBI, Natick, MA); R(1)arachidonyl-19-hydroxy-29-propylamide [R(1)-methanandamide] from Cayman Chemical Company (Ann Arbor, MI) or RBI (Natick, MA); v-agatoxin IVA, 8-bromo-cAMP, 3-isobutyl-1-methylxanthine (IBMX), 1-[6-((17b-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1Hpyrrole-2,5-dione (U-73122), 1-[6-((17b-3-methoxyestra-1,3,5(10)trien-17-yl)amino)hexyl]-2,5-pyrrolidine-dione (U-73343), pertussis toxin, Rp-adenosine 39,59-cyclic monophosphorothioate triethylamine (RpcAMPS), 9-(tetrahydro-29-furyl)adenine (SQ 22536), and xestospongin C from Calbiochem (San Diego, CA); and v-conotoxin GVIA from Peptides International (Louisville, KY) or Calbiochem.

Techniques: Control, MANN-WHITNEY